Increased Migration of Vascular Adventitial Fibroblasts from Spontaneously Hypertensive Rats

Li, Li; Zhu, Dingliang; Shen, Weili; Gao, Pingjin

doi:10.1291/hypres.29.95

Cited by 31 publications

(32 citation statements)

References 23 publications

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“…Following treatment, cells were washed with ice-cold PBS and lysed as described previously [25] . The protein concentration was determined by the Bradford method.…”

Section: Western Blot Analysismentioning

confidence: 99%

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Bao

2010

Acta Pharmacol Sin

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Aim: To investigate the protective effects of atorvastatin on homocysteine (Hcy)-induced dysfunction and apoptosis in endothelial progenitor cells (EPCs) and the possible molecular mechanisms. Methods: EPCs were divided into six groups: Hcy treatment groups (0, 50, and 500 μmol/L) and atorvastatin pretreatment groups (0.1, 1, and 10 μmol/L). EPC proliferation, migration, in vitro vasculogenesis activity, and apoptosis rate were assayed by the MTT assay, modified Boyden chamber assay, in vitro vasculogenesis kit, and AnnexinV-FITC apoptosis detection kit, respectively. The level of reactive oxygen species (ROS) in cells was measured using H 2 DCF-DA as a fluorescence probe. The activity of NADPH oxidase was evaluated with lucigenin-enhanced chemiluminescence. NO in the supernatant was detected by the nitrate reductase assay. The eNOS mRNA expression and p-eNOS, p-Akt, p-p38MAPK protein expression were measured by RT-PCR and Western blotting analysis, respectively. Caspase-3 activity was determined by colorimetric assay. Results: Hcy does-dependently impaired the proliferation, migration and in vitro vasculogenesis capacity of EPCs, induced cell apoptosis, increased ROS accumulation and NADPH oxidase activation, and decreased the secretion of NO compared with the control group (P<0.05 or P<0.01). The detrimental effects of Hcy were attenuated by atorvastatin pretreatment. Furthermore, Hcy caused a significant downregulation of eNOS mRNA, p-eNOS, and p-Akt protein expression as well as an upregulation of p-p38MAPK protein expression and caspase-3 activity. These effects of Hcy on EPCs were reversed by atorvastatin in a does-dependent manner. Conclusion: Atorvastatin inhibited homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells, which may be related to its effects on suppressing oxidative stress, up-regulating Akt/eNOS and down-regulating the p38MAPK/caspase-3 signaling pathway.

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“…Following treatment, cells were washed with ice-cold PBS and lysed as described previously [25] . The protein concentration was determined by the Bradford method.…”

Section: Western Blot Analysismentioning

confidence: 99%

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Bao

2010

Acta Pharmacol Sin

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“…Annexin A1 has been shown to modulate ERK but not p38 or JNK activity in lipopolysaccharride-induced responses [20] and regulate cell proliferation by disruption of cell morphology and inhibition of cyclin D1 expression through sustained activation of the ERK1/2 MAPK pathway [21] . Our previous studies showed that ERK1/2 was activated during phenotypic differentiation of AFs into MFs [22] and migration induced by Ang II [23] . Moreover, annexin A1 is a substrate for protein kinase C (PKC) and protein tyrosine kinases and has multiple phosphorylation sites as well as calcium and phospholipid binding properties.…”

Section: Discussionmentioning

confidence: 98%

“…Zhu [6] first found that spontaneously hypertensive rats (SHR)-AFs proliferated faster than Wistar Kyoto rats (WKY)-AFs, and increased cell density in the adventitia of stroke-prone SHR was revealed by confocal microscopy [7] . Moreover, we also found that the migration of SHR-AFs was always greater than that of WKY-AFs after treatment with various stimu lators [8,9] . Nevertheless, the mechanism of adventitial remodeling in SHR remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Dynamic expression of proteins associated with adventitial remodeling in adventitial fibroblasts from spontaneously hypertensive rats

et al. 2010

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Aim: To identify proteins that could potentially be involved in adventitial remodeling in vascular adventitial fibroblasts (AFs) from spontaneously hypertensive rats (SHR). Methods: AFs were isolated from thoracic aortas of 4-, 8-, 16-, and 24-week-old male SHR and Wistar-Kyoto (WKY) rats and cultured to passage 4. Proteomic differential expression profiles between SHR-AFs and WKY-AFs were investigated using 2-D electrophoresis (2-DE), whereas gel image analysis was processed using Image Master 2D Platinum. Protein spots were identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Expression levels of annexin A1 in AFs and aortas from SHR and WKY rats were detected with Western blotting and immunofluorescence techniques. Results: In 4-, 8-, 16-, and 24-week-old SHR-AFs, 49, 59, 54, and 69 protein spots were found to have significant differences from the age-matched WKY-AFs. Fourteen spots with the same changes in patterns were analyzed in 4-, 8-, 16-, and 24-week-old SHR-AFs with mass spectrometry. Except for cytoskeleton proteins such as tubulin beta 5, it was found that annexin A1, translation elongation factor Tu, endoplasmic reticulum protein 29 and calcium-binding protein 1 were expressed in vascular AFs and their levels changed significantly in SHR-AFs compared with those in WKY-AFs. A decrease in annexin A1 in SHR-AFs was confirmed with Western blotting and immunofluorescence staining at the cell and tissue levels. Conclusion: The application of proteomic techniques revealed a number of novel proteins involved in adventitial remodeling of AFs from SHR, which provide new mechanisms responsible for the occurrence and development of hypertension and potential targets for influencing vascular remodeling in hypertension.

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“…Following treatment, whole-cell lysates were prepared as described previously. 17) In some experiments, immunoblotting for CHOP protein was additionally performed on nuclear extracts prepared using a Nuclear Extraction Kit following the manufacturer's protocol (Millipore, Billerica, MA). The protein concentration was determined by the Lowry method.…”

Section: Measurementmentioning

confidence: 99%

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

Increased Migration of Vascular Adventitial Fibroblasts from Spontaneously Hypertensive Rats

Cited by 31 publications

References 23 publications

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Dynamic expression of proteins associated with adventitial remodeling in adventitial fibroblasts from spontaneously hypertensive rats

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

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