Spinal cord ischemia reperfusion injury (SCIRI) can cause spinal cord dysfunction and even devastating paraplegia. Calcium-sensing receptor (CaSR) and calpain are two calcium related molecules which have been reported to be involved in the ischemia reperfusion injury of cardiomyocytes and the subsequent apoptosis. Here, we studied the expression of CaSR and calpain in spinal cord neurons and tissues, followed by the further investigation of the role of CaSR/calpain axis in the cellular apoptosis process during SCIRI. The results of in vitro and in vivo studies showed that the expression of CaSR and calpain in spinal cord neurons increased during SCIRI. Moreover, the CaSR agonist GdCl and antagonist NPS-2390 enhanced or decreased the expression of CaSR and calpain respectively. The expressions of CaSR and calpain were also consistent with the cellular apoptosis in spinal cord. Taken together, CaSR-calpain contributes to the SCIRI apoptosis, and CaSR antagonist might be a helpful drug for alleviating SCIRI.
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http://dx.doi.org/10.1016/j.neulet.2017.03.009 | DOI Listing |
Arq Bras Cardiol
September 2021
The First People's Hospital of Guiyang, Guiyang - China.
Background: Cardiovascular disease is the major cause of death worldwide. Hypoxia-mediated apoptosis in cardiomyocytes is a major cause of cardiovascular disorders. Treatment with vascular endothelial growth factor (VEGF) protein has been tested but operational difficulties have limited its use.
View Article and Find Full Text PDFACS Appl Mater Interfaces
July 2018
Shanghai Biomaterials Research & Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People's Hospital , Shanghai Jiaotong University School of Medicine, Shanghai 200023 , China.
The development of nanomaterials for stable, controlled delivery of drugs and efficient suppression of tumor growth with desirable biosafety remains challenging in the nano-biomedical field. In this study, we prepared and optimized mesoporous bioactive glass (MBG) nanospheres to establish a functional drug delivery system and analyzed the effect of the dendritic mesoporous structure on drug loading and release. We then utilized an in vitro model to examine the biological effects of dendritic MBG nanospheres on normal and tumor cells and studied the molecular mechanism underlying specific tumor suppression by MBG nanospheres.
View Article and Find Full Text PDFNeurosci Lett
April 2017
Department of Orthopedic Surgery, Affiliated Hospital of Jiangsu University, Jiangsu, China.
Spinal cord ischemia reperfusion injury (SCIRI) can cause spinal cord dysfunction and even devastating paraplegia. Calcium-sensing receptor (CaSR) and calpain are two calcium related molecules which have been reported to be involved in the ischemia reperfusion injury of cardiomyocytes and the subsequent apoptosis. Here, we studied the expression of CaSR and calpain in spinal cord neurons and tissues, followed by the further investigation of the role of CaSR/calpain axis in the cellular apoptosis process during SCIRI.
View Article and Find Full Text PDFOncotarget
January 2017
Division of Hematology and Oncology, Department of Internal Medicine, School of Medicine, Saint Louis University, Saint Louis, MO 63104, USA.
Ca2+, a ubiquitous cellular signal, and filamin A, an actin-binding protein, play an important role in the regulation of cell adhesion, shape and motility. Using transwell filters to analyze cell migration, we found that extracellular Ca2+ (Cao2+) promotes the migration of androgen receptor (AR)-deficient and highly metastatic prostate cancer cell lines (DU145 and PC-3) compared to AR-positive and relatively less metastatic prostate cancer cells (LNCaP). Furthermore, we found that expression of filamin A is up-regulated in DU145 and PC-3 cells, and that Cao2+ significantly induces the cleavage of filamin A.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
June 2013
Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany.
The Ca-sensing receptor (CaSR) is expressed in endothelial and smooth muscle cells, but its role in regulating vascular reactivity is unclear, as are the effects of disease on CaSR function and expression. We studied vascular reactivity in aortic segments from healthy and diabetic mice, combined with in vitro proteolysis studies and Western blot analyses of CaSR expression in tissue samples. In endothelium-intact aortic rings, extracellular Ca elicited a nitric oxide-dependent relaxation that was attenuated by the CaSR antagonist, NPS2390.
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