Thrombospondin-1−induced vascular smooth muscle cell migration and proliferation are functionally dependent on microRNA-21

Stein, Jeffrey J.; Iwuchukwu, Chinenye; Maier, Kristopher G.; Gahtan, Vivian

doi:10.1016/j.surg.2013.08.003

Cited by 36 publications

(31 citation statements)

References 19 publications

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“…As a potent anti-angiogenic factor, TSP1 inhibits endothelial cell proliferation 49, 50 and migration 28, 51 and induces apoptosis 52, 53 . In vascular SMCs, TSP1 has been shown to promote proliferation and migration 54 . These diverse functions of TSP1 may differentially affect how the aortic wall responds to injuries associated with aneurysm.…”

Section: Discussionmentioning

confidence: 99%

Thrombospondin-1 (TSP1) Contributes to the Development of Vascular Inflammation by Regulating Monocytic Cell Motility in Mouse Models of Abdominal Aortic Aneurysm

Liu

Morgan

Ren

et al. 2015

Circulation Research

105

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Rationale Histological examination of abdominal aortic aneurysm (AAA) tissues demonstrates extracellular matrix (ECM) destruction and infiltration of inflammatory cells. Previous work with mouse models of AAA has shown that anti-inflammatory strategies can effectively attenuate aneurysm formation. Thrombospondin-1 (TSP1) is a matricellular protein involved in the maintenance of vascular structure and homeostasis through the regulation of biological functions such as cell proliferation, apoptosis, and adhesion. Expression levels of TSP1 correlate with vascular disease conditions. Objective To use TSP1 deficient (Thbs1−/−) mice to test the hypothesis that TSP1 contributes to pathogenesis of AAAs. Methods and Results Mouse experimental AAA was induced either through perivascular treatment with calcium phosphate, intraluminal perfusion with porcine elastase, or systemic administration of Angiotensin II. Induction of AAA increased TSP1 expression in aortas of C57BL/6 or apoE−/− mice. Compared to Thbs1+/+ mice, Thbs1−/− mice developed significantly smaller aortic expansion when subjected to AAA inductions, which was associated with diminished infiltration of macrophages. Thbs1−/− monocytic cells had reduced adhesion and migratory capacity in vitro compared to wildtype counterparts. Adoptive transfer of Thbs1+/+ monocytic cells or bone marrow reconstitution rescued aneurysm development in Thbs1−/− mice. Conclusions TSP1 expression plays a significant role in regulation of migration and adhesion of mononuclear cells, contributing to vascular inflammation during AAA development.

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Section: Discussionmentioning

confidence: 99%

Thrombospondin-1 (TSP1) Contributes to the Development of Vascular Inflammation by Regulating Monocytic Cell Motility in Mouse Models of Abdominal Aortic Aneurysm

Liu

Morgan

Ren

et al. 2015

Circulation Research

105

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“…19 Because TSP-1 was consistent with renal tubules damage after I/R injury, other contributive roles of miR-21 on TSP-1 remain to be investigated. In addition, it is interesting that Stein et al 39 indicated an active role for miR-21 in TSP1- ERK1/2 cell signaling cascade based on the finding that treatment with hyperglycemia and TSP-1 could stimulate the expression of miR-21. They could not confirm however the mechanism by which TSP-1 regulated the expression of miR-21.…”

Section: Discussionmentioning

confidence: 99%

Renal Protection Mediated by Hypoxia Inducible Factor-1α Depends on Proangiogenesis Function of miR-21 by Targeting Thrombospondin 1

Song

Zhang

et al. 2017

Transplantation

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BackgroundAngiogenesis contributes to the repair process after renal ischemia/reperfusion (I/R) injury. In the present study, we tested the role of miR-21 in the angiogenesis induced by hypoxia inducible factor (HIF)-1α through inhibiting a predicted target gene thrombospondin 1 (TSP-1).MethodsTo stabilize HIF-1α, hypoxia (1% O2 for 24 hours) was performed in human umbilical vein endothelial cells and cobalt chloride (CoCl2) was pretreated intraperitoneally 24 hours before renal I/R in mice. Locked nucleic acid modified anti-miR-21 and scrambled control was transfected with hypoxic cells or delivered into the mice via tail vein 1 hour before CoCl2 injection. The kidneys and blood were collected at 24 hours after reperfusion.ResultsHIF-1α induced by hypoxia and CoCl2 upregulated vascular endothelial growth factor and miR-21, and increased angiogenesis. It was found that expression of TSP-1 was inversely related with miR-21 in vitro and in vivo. Targeting of TSP-1 by miR-21 was further confirmed in vitro. Furthermore, HIF-1α improved renal function, accompanied with increased angiogenesis after I/R injury in mice. The protective effect of HIF-1α was attenuated by inhibition of miR-21.ConclusionsHIF-1α induced angiogenesis by upregulating not only vascular endothelial growth factor but also miR-21 via inhibiting a novel target gene TSP-1. Both of them may contribute to the protective effect of HIF-1α on renal I/R injury.

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“…Some miRNAs have been found to promote the proliferation and migration of VSMCs. miR-21 is one of the most abundant miRNAs in the vascular wall following balloon injury; it can enhance VSMCs migration and proliferation caused by TSP-1 [86] and stimulate the proliferation and migration of VSMCs through the suppression of c-Ski [83]. c-Ski is a molecule that is expressed in VSMCs to suppress VSMC stimulation and intimal hyperplasia in a rat balloon injury model [87].…”

Section: Mirnas and Vascular Agingmentioning

confidence: 99%

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin

Zhan

Wang

et al. 2016

BioMed Research International

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Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed.

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Thrombospondin-1−induced vascular smooth muscle cell migration and proliferation are functionally dependent on microRNA-21

Cited by 36 publications

References 19 publications

Thrombospondin-1 (TSP1) Contributes to the Development of Vascular Inflammation by Regulating Monocytic Cell Motility in Mouse Models of Abdominal Aortic Aneurysm

Thrombospondin-1 (TSP1) Contributes to the Development of Vascular Inflammation by Regulating Monocytic Cell Motility in Mouse Models of Abdominal Aortic Aneurysm

Renal Protection Mediated by Hypoxia Inducible Factor-1α Depends on Proangiogenesis Function of miR-21 by Targeting Thrombospondin 1

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

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