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Pericytes protect rats and mice from sepsis-induced injuries by maintaining vascular reactivity and barrier function:implication of miRNAs and microvesicles

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Military Medical Research 2024年第1期11卷 1-18页

作者： Zi-Sen Zhang Yi-Yan Liu Shuang-Shuang He Dai-Qin Bao Hong-Chen Wang Jie Zhang Xiao-Yong Peng Jia-Tao Zang Yu Zhu Yue Wu Qing-Hui Li Tao Li Liang-Ming Liu State Key Laboratory of Trauma Burns and Combined InjuryDepartment of Shock and TransfusionResearch Institute of SurgeryDaping HospitalArmy Medical UniversityChongqing 400042China

Background vascular hyporeactivity and leakage are key pathophysiologic features that produce multi-organ damage upon *** hypothesized that pericytes,a group of pluripotent cells that maintain vascular integrity and tension,are protective against sepsis via regulating vascular reactivity and *** We conducted a series of in vivo experiments using wild-type(WT),platelet-derived growth factor receptor-β(PDGFR-β)-Cre+mT/mG transgenic mice and Tie2-Cre+Cx43^(flox/flox)mice to examine the relative contribution of pericytes in sepsis,either induced by cecal ligation and puncture(CLP)or lipopolysaccharide(LPS)*** a separate set of experiments with Sprague-Dawley(SD)rats,pericytes were depleted using CP-673451,a selective PDGFR-βinhibitor,at a dosage of 40 mg/(kg·d)for 7 consecutive *** pericytes,vascular endothelial cells(VECs)and vascular smooth muscle cells(VSMCs)were used for mechanistic *** effects of pericytes and pericyte-derived microvesicles(PCMVs)and candidate miRNAs on vascular reactivity and barrier function were also *** CLP and LPS induced severe injury/loss of pericytes,vascular hyporeactivity and leakage(Pvascular reactivity and barrier function via microvessel colonization(Pvascular reactivity and barrier function after sepsis(Pvascular endothelial-cadherin *** Pericytes are protective a

关键词： Pericyte vascular reactivity vascular permeability Cx43 Microvesicle

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Beneficial effect of arginine vasopressin on hemorrhagic shock through improving the vascular reactivity

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Frontiers of Medicine 2008年第3期2卷 248-254页

作者： Tao LI Guangming YANG Jing XU Jiancang LIU Liangming LIU State Key Laboratory of Trauma Burns and Combined Injurythe 2nd Department of Research Institute of SurgeryDaping HospitalThird Military Medical UniversityChongqing 400042China

The vascular reactivity and calcium sensitivity were decreased following hemorrhagic *** vasopressin(AVP)was beneficial to endotoxic,infec-tious/septic and hemorrhagic *** previous studies found that Rho kinase played an important role in the occurrence of calcium desensitization following *** was reported that AVP was with stimulation effect of Rho *** we hypothesized that AVP might have bene-ficial effect on shock via activation of Rho kinase to regu-late the calcium sensitivity and vascular *** shock(40 mmHg for 2 h)Wistar rats in vivo were adopted to observe the effects of small dose of AVP on hemodynamics,24-h survival rate,the pressor effect of norepinephrine(NE)and the contractility of superior mesenteric artery(SMA).Isolated SMAs from hemorrha-gic shock rats were adopted to observe the effects of AVP on vascular reactivity and calcium sensitivity and its rela-tionship to Rho kinase with an isolated organ perfusion *** results show that AVP at the concentration of 0.1 U/kg and 0.4 U/kg significantly improved the hemo-dynamic parameters and the 24-h survival rate of hemor-rhagic shock ***,these dosages of AVP significantly increased the pressor effect of NE and the contractile response of SMA to NE.Y-27632(3 mg/kg),a Rho kinase specific inhibitor,abolished the beneficial effects of *** vitro,the calcium sensitivity and vas-cular reactivity of SMA to calcium and NE were signifi-cantly decreased following hemorrhagic *** at the concentration of 0.5 nmol/L and 5 nmol/L signifi-cantly increased the calcium sensitivity and vascular *** effects of AVP were abolished by Y-27632(10 mmol/L).Taken together,the results suggest that AVP at 0.1 U/kg and 0.4 U/kg is beneficial to hemorrha-gic shock by improving the vascular reactivity,which involves activation of Rho kinase.

关键词： hemorrhagic shock vascular reactivity cal-cium sensitivity Rho kinase arginine vasopressin

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vascular contractile response and signal transduction in endothelium-denuded aorta from cirrhotic rats

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World Journal of Gastroenterology 2005年第15期11卷 2306-2312页

作者： Han-ChiehLin Ying-YingYang Yi-TsauHuang Tzung-YanLee Ming-ChihHou Fa-YauhLee Shou-DongLee DivisionofGastroenterology DepartmentofMedicineTaipeiVeteransGeneralHospitalandNationalYang-MingUniversitySchoolofMedicineTaipeiTaiwanChina InstituteofClinicalMedicine NationalYang-MingUniversitySchoolofMedicineandTaipeiChung-HsiaoMunicipalHospitalTaipeiTaiwanChina InstituteofTraditionalMedicine Nafional.Yang-MingUniversitySchoolofMedicineTaipeiTaiwanChina

AIM: The mechanism of decreased vascular reactivity to vasoconstrictors in portal hypertension is still unclear. In addition to nitric oxide, defects in post-receptor signal transduction pathway have been suggested to play a ***, substantial evidences observed equivocal changes of vascular reactivity following different agonists that challenged the hypothesis of the post-receptor defect. The current study was to evaluate the vascular reactivity to different agonists and the inositol trisphosphate (IP3)changes in signal transduction cascade from cirrhotic rats with portal ***: The endothelial denuded aortic rings from cirrhotic and sham-operated rats were obtained for ex vivo tension study and measurement of the corresponding [3H] IP3 formation following different receptor and nonreceptor-mediated agonists' stimulation. Additionally,iNOS protein expression was measured in thoracic *** contractile response curves to phenylephrine were performed in endothelial denuded aortic rings with and without preincubation with a specific iNOS inhibitor (L-N (6)-(1-iminoethyl)-lysine, L-NIL).RESULTS: In endothelial denuded aortic rings of cirrhotic rats, the vascular responses were reduced with phenylephrine and arginine vasopressin (AVP) stimulation but were normal with U-46619, NaF/AlCl3, and phorbol esterdibutyrate (PdBU) stimulation. Compared to the corresponding control groups, the degree of the increment of [3H] IP3 formation from basal level was also decreased with phenylephrine and AVP stimulation, but was normal with U-46619 and NaF/AlCl3 stimulation. The preincubation with L-NIL did not modify the hyporesponsiveness to phenylephrine. Additionally, the iNOS protein expression in thoracic aorta was not different in cirrhotic and shamoperated ***: Without the influence of nitric oxide, vascular hyporeactivity to vasoconstrictors persisted in cirrhotic rats with portal hypertension. However, the decreased vascular reactivity is an

关键词： Cirrhosis Portal hypertension Inositol trisphosphate vascular reactivity Protein kinase C

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