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Parathyroid hormone-related protein (PTHrP)-dependent regulation of bcl-2 and tissue inhibitor of metalloproteinase (TIMP)-1 in coronary endothelial cells

, : Parathyroid hormone-related protein (PTHrP)-dependent regulation of bcl-2 and tissue inhibitor of metalloproteinase (TIMP)-1 in coronary endothelial cells. Cellular Physiology and Biochemistry 24(5-6): 493-502

An increased susceptibility of micro-vascular endothelial cells to apoptosis is considered to be an initial event leading to atherosclerosis. Parathyroid hormone-related peptide (PTHrP) is known to protect endothelial cells against apoptosis by the regulation of the anti-apoptotic gene bcl-2. As tissue inhibitor of metalloproteinase (TIMP-1) expression is regulated by bcl-2, we hypothesized that endothelial expression of PTHrP also regulates the expression of TIMP-1. The steady state mRNA expressions of bcl-2, bax, TIMP-1, and TIMP-2 were analyzed by real-time RT-PCR and their protein expression by immunoblotting. The tissue distribution of PTHrP was investigated in cryosections of hearts from normotensive and hypertensive rats. Phenylephrine, an alpha(1)-adrenoceptor agonist, increased the expression of PTHrP, bcl-2, and TIMP-1. Transfection of endothelial cells with oligonucleotides directed against PTHrP attenuated this effect. Antisense transfection and TGF-beta(1) (10 ng/ml) decreased the expression of PTHrP, bcl-2, TIMP-1, and TIMP-2, but not that of bax. Endothelial cells were identified as the main source of PTHrP in the heart. Endothelial cells in hearts from spontaneously hypertensive rats showed reduced staining with a PTHrP antibody compared to control normotensive hearts. These data suggests that the down-regulation of PTHrP favours atherosclerosis in chronic pressure overload.


PMID: 19910689

DOI: 10.1159/000257492

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