Faculty Appointments
Associate Professor of Pediatrics
Education
M.D., MEDICINE, George Washington University, Washington, District of ColumbiaB.S., University of Southern California, Los Angeles, California
Office Address
2200 Children's Way
5121 Doctors' Office Tower
Nashville, TN 37232
5121 Doctors' Office Tower
Nashville, TN 37232
Research Description
The purpose of my work is to understand the mechanisms through which acute inflammatory responses alter vascular function and contribute to critical illness. Further, I am interested in discovering ways that limit the negative impact inflammation has on the endothelium and associated vascular system. Previous work I have done has focused on the mechanisms involved in clot formation during exposure to endotoxin and cecal ligation and perforation, which are models of a severe infection known as sepsis. With this work, we found unique roles of complement 5a receptor and toll-like receptor 4 (TLR4) in endotoxin mediated microvascular thrombosis. My prior NIH research award was a continuation of this work on TLR4 mediated cellular activation, with a transition in emphasis from platelets to the endothelium. We investigated how endothelial cells are affected during infection, with specific focus on endothelial nitric oxide synthase (eNOS) dysfunction. Furthermore, we examined how priming of the immune system with a TLR4 agonist, monophosphoryl lipid a (MPLA), altered the pro-inflammatory responses of activated endothelial cells with secondary infectious challenges. These endeavors have continued in our current NIH-funded research program which broadly examines how multiple avenues of acute inflammation, both infectious and sterile, promote derangements in the vasculature.
While we have continued to explore eNOS, the primary endothelial producer of nitric oxide (NO), and how it directly interacts with a variety of inflammatory pathways in the endothelium, we have also developed interest in a group of metabolic regulators of inflammation, known as sirtuins (SIRTs). In particular, SIRT1, is known to modulate various aspects of metabolism and redox stress. We found that loss of SIRT1, which occurs during prolonged sepsis and with age, alters the metabolic phenotype of the endothelial cells to where they have a "metabolic shift" away from oxidative phosphorylation, the primary source of energy production, to glycolysis. This shift is associated with enhanced endothelial permeability and reduced vascular reactivity, suggesting that the loss of SIRT1, and the associated metabolic shift, can be quite detrimental to the vascular system in the setting of infectious challenge. What's more, we have demonstrated that eNOS and SIRT1 directly interact and co-localize with the structural endothelial protein, VE-Cadherin, putting eNOS-SIRT1 at the crossroads of endothelial permeability and metabolism.
Additionally, we have begun to explore endothelial dysfunction in humans using a technique called laser doppler perfusion monitoring which is couple to drug iontophoresis. This system allows us to test the function of the vasculature in critically ill patients using drugs that either stimulate the endothelial cells (acetylcholine) or the vascular smooth muscle cells (sodium nitroprusside). We have found in children undergoing either cardiopulmonary bypass for the correction of congenital heart surgery or those who present with sepsis, that endothelial-dependent vascular reactivity is more strongly impaired compared to endothelial-independent mechanisms, suggesting that the vascular dysfunction observed in critically ill children is primarily driven by endothelial dysfunction.
Our research program's long-term goal is to understand the mechanisms of acute vascular dysfunction and find modalities that allow for identification and future treatment. I have been involved in academic research throughout my career and have a passion to answer questions that arise in critically ill patients. I have also been involved in mentoring younger trainees with the hope of inspiring them to think critically and pose new and interesting questions on how we approach critical illness. Through the continuation of our research program, I hope to continue these pursuits by asking clinically relevant questions, investigating them with trainees in the laboratory and hospital settings, and ultimately finding answers that can be brought back to patients to help temper the severity of illness and reduce morbidity and mortality in the vulnerable population of pediatric critical illness.
Links:
https://news.vumc.org/2016/01/07/immune-tolerance-endothelial-cells/
https://news.vumc.org/2022/10/25/vascular-dysfunction-during-sepsis/
While we have continued to explore eNOS, the primary endothelial producer of nitric oxide (NO), and how it directly interacts with a variety of inflammatory pathways in the endothelium, we have also developed interest in a group of metabolic regulators of inflammation, known as sirtuins (SIRTs). In particular, SIRT1, is known to modulate various aspects of metabolism and redox stress. We found that loss of SIRT1, which occurs during prolonged sepsis and with age, alters the metabolic phenotype of the endothelial cells to where they have a "metabolic shift" away from oxidative phosphorylation, the primary source of energy production, to glycolysis. This shift is associated with enhanced endothelial permeability and reduced vascular reactivity, suggesting that the loss of SIRT1, and the associated metabolic shift, can be quite detrimental to the vascular system in the setting of infectious challenge. What's more, we have demonstrated that eNOS and SIRT1 directly interact and co-localize with the structural endothelial protein, VE-Cadherin, putting eNOS-SIRT1 at the crossroads of endothelial permeability and metabolism.
Additionally, we have begun to explore endothelial dysfunction in humans using a technique called laser doppler perfusion monitoring which is couple to drug iontophoresis. This system allows us to test the function of the vasculature in critically ill patients using drugs that either stimulate the endothelial cells (acetylcholine) or the vascular smooth muscle cells (sodium nitroprusside). We have found in children undergoing either cardiopulmonary bypass for the correction of congenital heart surgery or those who present with sepsis, that endothelial-dependent vascular reactivity is more strongly impaired compared to endothelial-independent mechanisms, suggesting that the vascular dysfunction observed in critically ill children is primarily driven by endothelial dysfunction.
Our research program's long-term goal is to understand the mechanisms of acute vascular dysfunction and find modalities that allow for identification and future treatment. I have been involved in academic research throughout my career and have a passion to answer questions that arise in critically ill patients. I have also been involved in mentoring younger trainees with the hope of inspiring them to think critically and pose new and interesting questions on how we approach critical illness. Through the continuation of our research program, I hope to continue these pursuits by asking clinically relevant questions, investigating them with trainees in the laboratory and hospital settings, and ultimately finding answers that can be brought back to patients to help temper the severity of illness and reduce morbidity and mortality in the vulnerable population of pediatric critical illness.
Links:
https://news.vumc.org/2016/01/07/immune-tolerance-endothelial-cells/
https://news.vumc.org/2022/10/25/vascular-dysfunction-during-sepsis/
Clinical Description
I am a member of the Pediatric Critical Care Division of Vanderbilt University School of Medicine. My clinical interests are related to my research endeavors, with specific interests in inflammatory responses related to infectious and traumatic injuries. In particular, I have a clinical interest in those patients who have protracted hospital courses related to continual immune dysfunction. This entity is known as persistent inflammation, immunosuppression and catabolism syndrome (PICS) and has been clearly linked with worse clinical outcomes in adult critically ill patients. We have found in pediatric critically ill patients, that this syndrome appears to arise more readily in patients who have undergone congenital heart disease surgery and is associated with a higher number of more severe infections. Our understanding of what contributes to this syndrome is just being to be explored, but it is clear that these patients have unique challenges and thus, require unique treatment modalities.
https://news.vumc.org/2023/06/29/persistent-inflammatory-state-found-in-half-of-pediatric-sepsis-deaths-study/
https://discoveries.vanderbilthealth.com/2024/01/no-one-size-fits-all-in-pediatric-sepsis/
https://news.vumc.org/2023/06/29/persistent-inflammatory-state-found-in-half-of-pediatric-sepsis-deaths-study/
https://discoveries.vanderbilthealth.com/2024/01/no-one-size-fits-all-in-pediatric-sepsis/
Research Keywords
Endothelial Dysfunction, Inflammation, Toll-like Receptors (TLR), Nitric Oxide (NO), Pediatric Critical Care, Sepsis, Metabolism
Clinical Research Keywords
Sepsis, Systemic Inflammatory Response Syndrome (SIRS), Burn Injury, Pediatric Critical Care, Pediatric Persistent Inflammation, Immunosuppression and Catabolism Syndrome (pPICS)
Publications
Lamb FS, Stark RJ. Smooth Muscle-Induced Endothelial Dysfunction in Obesity; Don't Just Blame the Middleman [editorial]. Circ Res [print-electronic]. 2025 Aug 8/29/2025; 137(6): 829-31. PMID: 40875794, DOI: 10.1161/CIRCRESAHA.125.327129, ISSN: 1524-4571.
Santarelli MD, Jeffery AD, Patterson SG, Kannankeril PJ, Slater ED, Wagner AL, Stark RJ. Persistent inflammation, immunosuppression, and catabolism syndrome and sepsis in pediatric burns. Burns [print-electronic]. 2025 Aug; 51(6): 107571. PMID: 40555121, PII: S0305-4179(25)00200-1, DOI: 10.1016/j.burns.2025.107571, ISSN: 1879-1409.
Stark RJ, Schrimpe-Rutledge AC, Codreanu SG, Sherrod SD, McLean JA, Krispinsky LT, Lamb FS. Endothelial-Dependent Vascular Reactivity After Cardiopulmonary Bypass is Associated with Unique Metabolomic Signatures. Shock [print-electronic]. 2024 Aug 8/12/2024; PMID: 39178242, PII: 00024382-990000000-00484, DOI: 10.1097/SHK.0000000000002446, ISSN: 1540-0514.
Santarelli MD, Davis KA, Stark RJ. Persistent Inflammation, Immunosuppression, and Catabolism Syndrome in Pediatric Populations: A Brief Perspective. Curr Pediatr Rev [print-electronic]. 2024 May 5/14/2024; PMID: 38752636, PII: CPR-EPUB-140353, DOI: 10.2174/0115733963298459240508050319, ISSN: 1875-6336.
Pourquoi A, Miller MR, Koch SR, Boyle K, Surratt V, Nguyen H, Panja S, Cartailler JP, Shrestha S, Stark RJ. DIFFERENTIAL SIGNALING EFFECTS OF ESCHERICHIA COLI AND STAPHYLOCOCCUS AUREUS IN HUMAN WHOLE BLOOD INDICATE DISTINCT REGULATION OF THE NRF2 PATHWAY. Shock [print-electronic]. 2024 Apr 4/1/2024; 61(4): 557-63. PMID: 38604133, PMCID: PMC11018340, PII: 00024382-202404000-00008, DOI: 10.1097/SHK.0000000000002305, ISSN: 1540-0514.
Lamb FS, Choi H, Miller MR, Stark RJ. Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels. Hypertension [print-electronic]. 2024 Jan 1/4/2024; PMID: 38174563, DOI: 10.1161/HYPERTENSIONAHA.123.19434, ISSN: 1524-4563.
Choi H, Miller MR, Nguyen HN, Surratt VE, Koch SR, Stark RJ, Lamb FS. Extracellular SOD modulates canonical TNFa signaling and a5ß1 integrin transactivation in vascular smooth muscle cells. Free Radic Biol Med [print-electronic]. 2023 Oct 10/16/2023; 209(Pt 1): 152-64. PMID: 37852546, PII: S0891-5849(23)01069-9, DOI: 10.1016/j.freeradbiomed.2023.10.397, ISSN: 1873-4596.
Choi H, Miller MR, Nguyen HN, Rohrbough JC, Koch SR, Boatwright N, Yarboro MT, Sah R, McDonald WH, Reese JJ, Stark RJ, Lamb FS. LRRC8A anion channels modulate vascular reactivity via association with myosin phosphatase rho interacting protein. FASEB J. 2023 Jul; 37(7): e23028. PMID: 37310356, DOI: 10.1096/fj.202300561R, ISSN: 1530-6860.
Patterson SG, Lamb CK, Gong W, Resser J, Lindsell CJ, Van Driest SL, Stark RJ. Pediatric Persistent Inflammation, Immunosuppression, and Catabolism Syndrome Prevalence in Sepsis-Related Mortalities: A 23-Year Institutional History. Chest [print-electronic]. 2023 May 5/8/2023; PMID: 37164130, PII: S0012-3692(23)00651-7, DOI: 10.1016/j.chest.2023.05.002, ISSN: 1931-3543.
Choi H, Miller MR, Nguyen HN, Rohrbough JC, Koch SR, Boatwright N, Yarboro MT, Sah R, McDonald WH, Reese JJ, Stark RJ, Lamb FS. LRRC8A anion channels modulate vasodilation via association with Myosin Phosphatase Rho Interacting Protein (MPRIP). BioRxiv. 2023 Mar 3/10/2023; PMID: 36945623, PMCID: PMC10028897, PII: 2023.03.08.531807, DOI: 10.1101/2023.03.08.531807.
Stark RJ, Yildizdas D. Editorial: Case reports in pediatric critical care 2022 [editorial]. Front Pediatr. 2023; 11: 1176704. PMID: 37009277, PMCID: PMC10064131, DOI: 10.3389/fped.2023.1176704, ISSN: 2296-2360.
Stark R. Protein-mediated interactions in the dynamic regulation of acute inflammation. Biocell [print-electronic]. 2023; 47(6): 1191-8. PMID: 37261220, PMCID: PMC10231872, DOI: 10.32604/biocell.2023.027838, ISSN: 0327-9545.
Stark RJ, Nguyen HN, Bacon MK, Rohrbough JC, Choi H, Lamb FS. Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels. J Membr Biol [print-electronic]. 2022 Nov 11/2/2022; PMID: 36322172, PII: 10.1007/s00232-022-00271-9, DOI: 10.1007/s00232-022-00271-9, ISSN: 1432-1424.
Stark RJ, Koch SR, Stothers CL, Pourquoi A, Lamb CK, Miller MR, Choi H. Loss of Sirtuin 1 (SIRT1) potentiates endothelial dysfunction via impaired glycolysis during infectious challenge [letter]. Clin Transl Med. 2022 Sep; 12(9): e1054. PMID: 36103428, PMCID: PMC9473483, DOI: 10.1002/ctm2.1054, ISSN: 2001-1326.
Stark RJ. Endothelial-Dependent Responses Correlate with Pediatric SOFA Scores During Severe Sepsis and Septic Shock. J Cardiovasc Transl Res [print-electronic]. 2022 Jan 1/17/2022; PMID: 35040080, PII: 10.1007/s12265-021-10202-z, DOI: 10.1007/s12265-021-10202-z, ISSN: 1937-5395.
Wijers CDM, Stark RJ. Case report: Temporal alterations in vascular function during the first 2 weeks of pediatric septic shock. Front Pediatr. 2022; 10: 939886. PMID: 35935367, PMCID: PMC9354618, DOI: 10.3389/fped.2022.939886, ISSN: 2296-2360.
Koch SR, Stark RJ. Cell penetrating peptides coupled to an endothelial nitric oxide synthase sequence alter endothelial permeability. Tissue Barriers [print-electronic]. 2021 Dec 12/18/2021; 2017226. PMID: 34923902, DOI: 10.1080/21688370.2021.2017226, ISSN: 2168-8370.
Miller MR, Koch SR, Choi H, Lamb FS, Stark RJ. Apoptosis Signal-Regulating Kinase 1 (ASK1) Inhibition Reduces Endothelial Cytokine Production without Improving Permeability after Toll-like Receptor 4 (TLR4) Challenge. Transl Res [print-electronic]. 2021 Apr 4/12/2021; PMID: 33857660, PII: S1931-5244(21)00083-9, DOI: 10.1016/j.trsl.2021.04.001, ISSN: 1878-1810.
Stark RJ, Krispinsky LT, Lamb FS. The Inverse Relationship Between Endothelium-Dependent Vasodilation and Blood Pressure is Lost After Cardiopulmonary Bypass. J Cardiovasc Transl Res [print-electronic]. 2021 Apr 4/9/2021; PMID: 33835431, PII: 10.1007/s12265-021-10124-w, DOI: 10.1007/s12265-021-10124-w, ISSN: 1937-5395.
Lamb FS, Choi H, Miller MR, Stark RJ. TNFa and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis. Am. J. Hypertens [print-electronic]. 2020 Jun 6/5/2020; PMID: 32498083, PII: 5851521, DOI: 10.1093/ajh/hpaa089, ISSN: 1941-7225.
Stark RJ, Choi H, Lamb FS. Neuronal ASIC1A As a Cerebral pH Sensor: Bringing the Flow [editorial]. Circ. Res [print-electronic]. 2019 Oct 10/25/2019; 125(10): 921-3. PMID: 31647772, PMCID: PMC6993881, DOI: 10.1161/CIRCRESAHA.119.315925, ISSN: 1524-4571.
Krispinsky LT, Stark RJ, Parra DA, Luan L, Bichell DP, Pietsch JB, Lamb FS. Endothelial-Dependent Vasomotor Dysfunction in Infants After Cardiopulmonary Bypass. Pediatr Crit Care Med [print-electronic]. 2019 Jun 6/26/2019; PMID: 31246738, DOI: 10.1097/PCC.0000000000002049, ISSN: 1529-7535.
Fukuda S, Ihara K, Bohannon JK, Hernandez A, Patil NK, Luan L, Stothers C, Stark R, Prough DS, Herndon DN, Sherwood ER, Enkhbaatar P. Monophosphoryl Lipid A Attenuates Multiorgan Dysfunction During Post-Burn Pseudomonas Aeruginosa Pneumonia In Sheep. Shock [print-electronic]. 2019 Apr 4/26/2019; PMID: 31045990, DOI: 10.1097/SHK.0000000000001364, ISSN: 1540-0514.
Thompson KB, Krispinsky LT, Stark RJ. Late immune consequences of combat trauma: a review of trauma-related immune dysfunction and potential therapies. Mil Med Res. 2019 Apr 4/24/2019; 6(1): 11. PMID: 31014397, PMCID: PMC6480837, PII: 10.1186/s40779-019-0202-0, DOI: 10.1186/s40779-019-0202-0, ISSN: 2054-9369.
Koch SR, Choi H, Mace EH, Stark RJ. Toll-like receptor 3-mediated inflammation by p38 is enhanced by endothelial nitric oxide synthase knockdown. Cell Commun. Signal. 2019 Apr 4/15/2019; 17(1): 33. PMID: 30987646, PMCID: PMC6466662, PII: 10.1186/s12964-019-0345-3, DOI: 10.1186/s12964-019-0345-3, ISSN: 1478-811X.
Choi H, Stark RJ, Raja BS, Dikalova A, Lamb FS. Apoptosis signal-regulating kinase 1 activation by Nox1-derived oxidants is required for TNFa receptor endocytosis. Am. J. Physiol. Heart Circ. Physiol [print-electronic]. 2019 Mar 3/29/2019; PMID: 30925081, DOI: 10.1152/ajpheart.00741.2018, ISSN: 1522-1539.
Stark RJ, Koch SR, Choi H, Mace EH, Dikalov SI, Sherwood ER, Lamb FS. Endothelial nitric oxide synthase modulates Toll-like receptor 4-mediated IL-6 production and permeability via nitric oxide-independent signaling. FASEB J [print-electronic]. 2017 Oct 10/23/2017; PMID: 29061842, PII: fj.201700410R, DOI: 10.1096/fj.201700410R, ISSN: 1530-6860.
Luan L, Patil NK, Guo Y, Hernandez A, Bohannon JK, Fensterheim BA, Wang J, Xu Y, Enkhbaatar P, Stark R, Sherwood ER. Comparative Transcriptome Profiles of Human Blood in Response to the Toll-like Receptor 4 Ligands Lipopolysaccharide and Monophosphoryl Lipid A. Sci Rep. 2017 Jan 1/5/2017; 7: 40050. PMID: 28053314, PII: srep40050, DOI: 10.1038/srep40050, ISSN: 2045-2322.
Koch SR, Lamb FS, Hellman J, Sherwood ER, Stark RJ. Potentiation and tolerance of toll-like receptor priming in human endothelial cells. Transl Res [print-electronic]. 2016 Aug 8/8/2016; PMID: 27567430, PII: S1931-5244(16)30158-X, DOI: 10.1016/j.trsl.2016.08.001, ISSN: 1878-1810.
Stark RJ, Choi H, Koch SR, Fensterheim BA, Lamb FS, Sherwood ER. Endothelial cell tolerance to lipopolysaccharide challenge is induced by Monophosphoryl lipid A. Clin. Sci [print-electronic]. 2015 Dec 12/15/2015; PMID: 26669797, PII: CS20150592, DOI: 10.1042/CS20150592, ISSN: 1470-8736.
Choi H, Dikalova A, Stark RJ, Lamb FS. C-Jun N-terminal kinase attenuates TNFa signaling by reducing Nox1-dependent endosomal ROS production in vascular smooth muscle cells. Free Radic. Biol. Med [print-electronic]. 2015 Sep; 86: 219-27. PMID: 26001727, PII: S0891-5849(15)00226-9, DOI: 10.1016/j.freeradbiomed.2015.05.015, ISSN: 1873-4596.
Stark R, Choi H, Koch S, Lamb F, Sherwood E. Monophosphoryl lipid A inhibits the cytokine response of endothelial cells challenged with LPS. Innate Immun [print-electronic]. 2015 Aug; 21(6): 565-74. PMID: 25540284, PMCID: PMC4480205, PII: 1753425914564172, DOI: 10.1177/1753425914564172, ISSN: 1753-4267.
Stark RJ, Shekerdemian LS. Estimating intracardiac and extracardiac shunting in the setting of complex congenital heart disease. Ann Pediatr Cardiol. 2013 Jul; 6(2): 145-51. PMID: 24688231, PMCID: PMC3957443, PII: APC-6-145, DOI: 10.4103/0974-2069.115259, ISSN: 0974-2069.
Stark RJ, Naik-Mathuria BJ, Lam FW, Olutoye OO, Sutton VR, Shekerdemian LS. Extracorporeal membrane oxygenation support of a severe metabolic crisis in a child with methylmalonic acidemia. ASAIO J. 2012 Jul; 58(4): 438-9. PMID: 22711065, DOI: 10.1097/MAT.0b013e31825a223c, ISSN: 1538-943X.
Stark RJ, Aghakasiri N, Rumbaut RE. Platelet-derived Toll-like receptor 4 (Tlr-4) is sufficient to promote microvascular thrombosis in endotoxemia. PLoS ONE [print-electronic]. 2012; 7(7): e41254. PMID: 22911769, PMCID: PMC3401143, PII: PONE-D-12-14054, DOI: 10.1371/journal.pone.0041254, ISSN: 1932-6203.
Shen W, Falahati R, Stark R, Leitenberg D, Ladisch S. Modulation of CD4 Th cell differentiation by ganglioside GD1a in vitro. J. Immunol. 2005 Oct 10/15/2005; 175(8): 4927-34. PMID: 16210594, PII: 175/8/4927, ISSN: 0022-1767.
Santarelli MD, Jeffery AD, Patterson SG, Kannankeril PJ, Slater ED, Wagner AL, Stark RJ. Persistent inflammation, immunosuppression, and catabolism syndrome and sepsis in pediatric burns. Burns [print-electronic]. 2025 Aug; 51(6): 107571. PMID: 40555121, PII: S0305-4179(25)00200-1, DOI: 10.1016/j.burns.2025.107571, ISSN: 1879-1409.
Stark RJ, Schrimpe-Rutledge AC, Codreanu SG, Sherrod SD, McLean JA, Krispinsky LT, Lamb FS. Endothelial-Dependent Vascular Reactivity After Cardiopulmonary Bypass is Associated with Unique Metabolomic Signatures. Shock [print-electronic]. 2024 Aug 8/12/2024; PMID: 39178242, PII: 00024382-990000000-00484, DOI: 10.1097/SHK.0000000000002446, ISSN: 1540-0514.
Santarelli MD, Davis KA, Stark RJ. Persistent Inflammation, Immunosuppression, and Catabolism Syndrome in Pediatric Populations: A Brief Perspective. Curr Pediatr Rev [print-electronic]. 2024 May 5/14/2024; PMID: 38752636, PII: CPR-EPUB-140353, DOI: 10.2174/0115733963298459240508050319, ISSN: 1875-6336.
Pourquoi A, Miller MR, Koch SR, Boyle K, Surratt V, Nguyen H, Panja S, Cartailler JP, Shrestha S, Stark RJ. DIFFERENTIAL SIGNALING EFFECTS OF ESCHERICHIA COLI AND STAPHYLOCOCCUS AUREUS IN HUMAN WHOLE BLOOD INDICATE DISTINCT REGULATION OF THE NRF2 PATHWAY. Shock [print-electronic]. 2024 Apr 4/1/2024; 61(4): 557-63. PMID: 38604133, PMCID: PMC11018340, PII: 00024382-202404000-00008, DOI: 10.1097/SHK.0000000000002305, ISSN: 1540-0514.
Lamb FS, Choi H, Miller MR, Stark RJ. Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels. Hypertension [print-electronic]. 2024 Jan 1/4/2024; PMID: 38174563, DOI: 10.1161/HYPERTENSIONAHA.123.19434, ISSN: 1524-4563.
Choi H, Miller MR, Nguyen HN, Surratt VE, Koch SR, Stark RJ, Lamb FS. Extracellular SOD modulates canonical TNFa signaling and a5ß1 integrin transactivation in vascular smooth muscle cells. Free Radic Biol Med [print-electronic]. 2023 Oct 10/16/2023; 209(Pt 1): 152-64. PMID: 37852546, PII: S0891-5849(23)01069-9, DOI: 10.1016/j.freeradbiomed.2023.10.397, ISSN: 1873-4596.
Choi H, Miller MR, Nguyen HN, Rohrbough JC, Koch SR, Boatwright N, Yarboro MT, Sah R, McDonald WH, Reese JJ, Stark RJ, Lamb FS. LRRC8A anion channels modulate vascular reactivity via association with myosin phosphatase rho interacting protein. FASEB J. 2023 Jul; 37(7): e23028. PMID: 37310356, DOI: 10.1096/fj.202300561R, ISSN: 1530-6860.
Patterson SG, Lamb CK, Gong W, Resser J, Lindsell CJ, Van Driest SL, Stark RJ. Pediatric Persistent Inflammation, Immunosuppression, and Catabolism Syndrome Prevalence in Sepsis-Related Mortalities: A 23-Year Institutional History. Chest [print-electronic]. 2023 May 5/8/2023; PMID: 37164130, PII: S0012-3692(23)00651-7, DOI: 10.1016/j.chest.2023.05.002, ISSN: 1931-3543.
Choi H, Miller MR, Nguyen HN, Rohrbough JC, Koch SR, Boatwright N, Yarboro MT, Sah R, McDonald WH, Reese JJ, Stark RJ, Lamb FS. LRRC8A anion channels modulate vasodilation via association with Myosin Phosphatase Rho Interacting Protein (MPRIP). BioRxiv. 2023 Mar 3/10/2023; PMID: 36945623, PMCID: PMC10028897, PII: 2023.03.08.531807, DOI: 10.1101/2023.03.08.531807.
Stark RJ, Yildizdas D. Editorial: Case reports in pediatric critical care 2022 [editorial]. Front Pediatr. 2023; 11: 1176704. PMID: 37009277, PMCID: PMC10064131, DOI: 10.3389/fped.2023.1176704, ISSN: 2296-2360.
Stark R. Protein-mediated interactions in the dynamic regulation of acute inflammation. Biocell [print-electronic]. 2023; 47(6): 1191-8. PMID: 37261220, PMCID: PMC10231872, DOI: 10.32604/biocell.2023.027838, ISSN: 0327-9545.
Stark RJ, Nguyen HN, Bacon MK, Rohrbough JC, Choi H, Lamb FS. Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels. J Membr Biol [print-electronic]. 2022 Nov 11/2/2022; PMID: 36322172, PII: 10.1007/s00232-022-00271-9, DOI: 10.1007/s00232-022-00271-9, ISSN: 1432-1424.
Stark RJ, Koch SR, Stothers CL, Pourquoi A, Lamb CK, Miller MR, Choi H. Loss of Sirtuin 1 (SIRT1) potentiates endothelial dysfunction via impaired glycolysis during infectious challenge [letter]. Clin Transl Med. 2022 Sep; 12(9): e1054. PMID: 36103428, PMCID: PMC9473483, DOI: 10.1002/ctm2.1054, ISSN: 2001-1326.
Stark RJ. Endothelial-Dependent Responses Correlate with Pediatric SOFA Scores During Severe Sepsis and Septic Shock. J Cardiovasc Transl Res [print-electronic]. 2022 Jan 1/17/2022; PMID: 35040080, PII: 10.1007/s12265-021-10202-z, DOI: 10.1007/s12265-021-10202-z, ISSN: 1937-5395.
Wijers CDM, Stark RJ. Case report: Temporal alterations in vascular function during the first 2 weeks of pediatric septic shock. Front Pediatr. 2022; 10: 939886. PMID: 35935367, PMCID: PMC9354618, DOI: 10.3389/fped.2022.939886, ISSN: 2296-2360.
Koch SR, Stark RJ. Cell penetrating peptides coupled to an endothelial nitric oxide synthase sequence alter endothelial permeability. Tissue Barriers [print-electronic]. 2021 Dec 12/18/2021; 2017226. PMID: 34923902, DOI: 10.1080/21688370.2021.2017226, ISSN: 2168-8370.
Miller MR, Koch SR, Choi H, Lamb FS, Stark RJ. Apoptosis Signal-Regulating Kinase 1 (ASK1) Inhibition Reduces Endothelial Cytokine Production without Improving Permeability after Toll-like Receptor 4 (TLR4) Challenge. Transl Res [print-electronic]. 2021 Apr 4/12/2021; PMID: 33857660, PII: S1931-5244(21)00083-9, DOI: 10.1016/j.trsl.2021.04.001, ISSN: 1878-1810.
Stark RJ, Krispinsky LT, Lamb FS. The Inverse Relationship Between Endothelium-Dependent Vasodilation and Blood Pressure is Lost After Cardiopulmonary Bypass. J Cardiovasc Transl Res [print-electronic]. 2021 Apr 4/9/2021; PMID: 33835431, PII: 10.1007/s12265-021-10124-w, DOI: 10.1007/s12265-021-10124-w, ISSN: 1937-5395.
Lamb FS, Choi H, Miller MR, Stark RJ. TNFa and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis. Am. J. Hypertens [print-electronic]. 2020 Jun 6/5/2020; PMID: 32498083, PII: 5851521, DOI: 10.1093/ajh/hpaa089, ISSN: 1941-7225.
Stark RJ, Choi H, Lamb FS. Neuronal ASIC1A As a Cerebral pH Sensor: Bringing the Flow [editorial]. Circ. Res [print-electronic]. 2019 Oct 10/25/2019; 125(10): 921-3. PMID: 31647772, PMCID: PMC6993881, DOI: 10.1161/CIRCRESAHA.119.315925, ISSN: 1524-4571.
Krispinsky LT, Stark RJ, Parra DA, Luan L, Bichell DP, Pietsch JB, Lamb FS. Endothelial-Dependent Vasomotor Dysfunction in Infants After Cardiopulmonary Bypass. Pediatr Crit Care Med [print-electronic]. 2019 Jun 6/26/2019; PMID: 31246738, DOI: 10.1097/PCC.0000000000002049, ISSN: 1529-7535.
Fukuda S, Ihara K, Bohannon JK, Hernandez A, Patil NK, Luan L, Stothers C, Stark R, Prough DS, Herndon DN, Sherwood ER, Enkhbaatar P. Monophosphoryl Lipid A Attenuates Multiorgan Dysfunction During Post-Burn Pseudomonas Aeruginosa Pneumonia In Sheep. Shock [print-electronic]. 2019 Apr 4/26/2019; PMID: 31045990, DOI: 10.1097/SHK.0000000000001364, ISSN: 1540-0514.
Thompson KB, Krispinsky LT, Stark RJ. Late immune consequences of combat trauma: a review of trauma-related immune dysfunction and potential therapies. Mil Med Res. 2019 Apr 4/24/2019; 6(1): 11. PMID: 31014397, PMCID: PMC6480837, PII: 10.1186/s40779-019-0202-0, DOI: 10.1186/s40779-019-0202-0, ISSN: 2054-9369.
Koch SR, Choi H, Mace EH, Stark RJ. Toll-like receptor 3-mediated inflammation by p38 is enhanced by endothelial nitric oxide synthase knockdown. Cell Commun. Signal. 2019 Apr 4/15/2019; 17(1): 33. PMID: 30987646, PMCID: PMC6466662, PII: 10.1186/s12964-019-0345-3, DOI: 10.1186/s12964-019-0345-3, ISSN: 1478-811X.
Choi H, Stark RJ, Raja BS, Dikalova A, Lamb FS. Apoptosis signal-regulating kinase 1 activation by Nox1-derived oxidants is required for TNFa receptor endocytosis. Am. J. Physiol. Heart Circ. Physiol [print-electronic]. 2019 Mar 3/29/2019; PMID: 30925081, DOI: 10.1152/ajpheart.00741.2018, ISSN: 1522-1539.
Stark RJ, Koch SR, Choi H, Mace EH, Dikalov SI, Sherwood ER, Lamb FS. Endothelial nitric oxide synthase modulates Toll-like receptor 4-mediated IL-6 production and permeability via nitric oxide-independent signaling. FASEB J [print-electronic]. 2017 Oct 10/23/2017; PMID: 29061842, PII: fj.201700410R, DOI: 10.1096/fj.201700410R, ISSN: 1530-6860.
Luan L, Patil NK, Guo Y, Hernandez A, Bohannon JK, Fensterheim BA, Wang J, Xu Y, Enkhbaatar P, Stark R, Sherwood ER. Comparative Transcriptome Profiles of Human Blood in Response to the Toll-like Receptor 4 Ligands Lipopolysaccharide and Monophosphoryl Lipid A. Sci Rep. 2017 Jan 1/5/2017; 7: 40050. PMID: 28053314, PII: srep40050, DOI: 10.1038/srep40050, ISSN: 2045-2322.
Koch SR, Lamb FS, Hellman J, Sherwood ER, Stark RJ. Potentiation and tolerance of toll-like receptor priming in human endothelial cells. Transl Res [print-electronic]. 2016 Aug 8/8/2016; PMID: 27567430, PII: S1931-5244(16)30158-X, DOI: 10.1016/j.trsl.2016.08.001, ISSN: 1878-1810.
Stark RJ, Choi H, Koch SR, Fensterheim BA, Lamb FS, Sherwood ER. Endothelial cell tolerance to lipopolysaccharide challenge is induced by Monophosphoryl lipid A. Clin. Sci [print-electronic]. 2015 Dec 12/15/2015; PMID: 26669797, PII: CS20150592, DOI: 10.1042/CS20150592, ISSN: 1470-8736.
Choi H, Dikalova A, Stark RJ, Lamb FS. C-Jun N-terminal kinase attenuates TNFa signaling by reducing Nox1-dependent endosomal ROS production in vascular smooth muscle cells. Free Radic. Biol. Med [print-electronic]. 2015 Sep; 86: 219-27. PMID: 26001727, PII: S0891-5849(15)00226-9, DOI: 10.1016/j.freeradbiomed.2015.05.015, ISSN: 1873-4596.
Stark R, Choi H, Koch S, Lamb F, Sherwood E. Monophosphoryl lipid A inhibits the cytokine response of endothelial cells challenged with LPS. Innate Immun [print-electronic]. 2015 Aug; 21(6): 565-74. PMID: 25540284, PMCID: PMC4480205, PII: 1753425914564172, DOI: 10.1177/1753425914564172, ISSN: 1753-4267.
Stark RJ, Shekerdemian LS. Estimating intracardiac and extracardiac shunting in the setting of complex congenital heart disease. Ann Pediatr Cardiol. 2013 Jul; 6(2): 145-51. PMID: 24688231, PMCID: PMC3957443, PII: APC-6-145, DOI: 10.4103/0974-2069.115259, ISSN: 0974-2069.
Stark RJ, Naik-Mathuria BJ, Lam FW, Olutoye OO, Sutton VR, Shekerdemian LS. Extracorporeal membrane oxygenation support of a severe metabolic crisis in a child with methylmalonic acidemia. ASAIO J. 2012 Jul; 58(4): 438-9. PMID: 22711065, DOI: 10.1097/MAT.0b013e31825a223c, ISSN: 1538-943X.
Stark RJ, Aghakasiri N, Rumbaut RE. Platelet-derived Toll-like receptor 4 (Tlr-4) is sufficient to promote microvascular thrombosis in endotoxemia. PLoS ONE [print-electronic]. 2012; 7(7): e41254. PMID: 22911769, PMCID: PMC3401143, PII: PONE-D-12-14054, DOI: 10.1371/journal.pone.0041254, ISSN: 1932-6203.
Shen W, Falahati R, Stark R, Leitenberg D, Ladisch S. Modulation of CD4 Th cell differentiation by ganglioside GD1a in vitro. J. Immunol. 2005 Oct 10/15/2005; 175(8): 4927-34. PMID: 16210594, PII: 175/8/4927, ISSN: 0022-1767.