By M. Sahay
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Additional resources for Chronic Kidney Disease and Renal Transplantation
2005). Recent data strongly suggest that PTHrP might be involved in the mechanisms related to Ang II-induced renal injury. , 1993). , 2002). , 2005). Collectively, current data suggest that: 1) Ang II is a likely candidate responsible for PTHrP overexpression; and 2) PTHrP might contribute to the deleterious effects of Ang II, in the damaged kidney. These findings have established a new rationale for further studies focused on the putative contribution of PTHrP to the mechanisms of renal damage.
Taken together, these data suggest that PTHrP might mediate the hypertrophic signalling acting in an autocrine/intracrine fashion through the PTH1R receptor. To discern the mechanism involved in the stimulation of p27kip1 induced by both PTHrP and TGF-β1, Romero et al (2010) performed two experimental approaches. First, they found that using a PTHrP siRNA inhibited the ability of HG and AngII to stimulate the upregulation of p27Kip1, albeit it could not prevent the TGF-β1 upregulation of this protein.
JAMA 1980; 244: 2532-5  Jones MR, Sealey JE, Laragh JH: Effects of angiotensin receptor blockers on ambulatory plasma Renin activity in healthy, normal subjects during unrestricted sodium intake. Am J Hypertens 2007; 20: 907-16  Alderman MH, Ooi WL, Cohen H, Madhavan S, Sealey JE, Laragh JH: Plasma renin activity: a risk factor for myocardial infarction in hypertensive patients. Am J Hypertens 1997; 10: 1-8  Latini R, Masson S, Anand I, Salio M, Hester A, Judd D, Barlera S, Maggioni AP, Tognoni G, Cohn JN: The comparative prognostic value of plasma neurohormones at baseline in patients with heart failure enrolled in Val-HeFT.