Office address

Integrative Biosciences Building
iBIO-1413
6435 Woodward, Detroit MI

 

Areas of interest

Renal Physiology, Obesity, Diabetes, and Hypertension

Narrative bio

During my PhD training I worked with primary cultures of cardiomyocytes. I acquired experience in molecular biology techniques to study signaling mechanisms controlling cardiac hypertrophy in cells as well as whole animal physiology to understand the role of prostaglandins in remodeling and cardiac infarction. I have been particularly thrilled with how processes occurring at a very small scale govern cell structure and function. Since then I have studied the pathobiology of hypertension, from heart to kidney, and from molecule to whole animal models.

Our work for the past ~10 years has focused on understanding the mechanisms of renin biology and release. The field of renin biology has been understudied at a molecular level. This is in part due to the lack of technological developments to either isolate or study cells that produce and release renin. This has impaired the ability to advance the knowledge on very basic mechanisms of renin biology. When compared to the advances in the knowledge on other endocrine secretory cells, such as insulin-secreting pancreatic cells, the field of renin is very behind, preventing the development of better targets for the treatment of hypertension.

• Regulation of SNARE-dependent renin granule exocytosis: The major role of this project is to understand the mechanisms of renin granule exocytosis, stimulated by cAMP and identification of the proteins involved.
• ROS dependent-stimulated Renin release: role Hypertension and Diabetic nephropathy: Hypertension affects up to 50% of patients with type 1 diabetes (20-25 million in the US), speeding up the progression of kidney dysfunction. The pathogenesis of hypertension in diabetes involves the activation of the renin-angiotensin system (RAS). Renin is the rate-limiting enzyme in the activation of the RAS and is essential for blood pressure control. The only source of the circulating hormone renin is the renal microcirculation, specifically Juxtaglomerular Cells (JG cells) where renin is expressed as an immature pro-peptide ((pro)renin). However, in type 1 diabetes higher plasma (pro)renin and increased intra-renal renin are associated with hypertension and kidney dysfunction. The mechanisms by which diabetes enhances plasma (pro)renin and intrarenal renin are not clear. While it is well established that the renin-angiotensin system is activated in diabetes and contributes to hypertension, the role of the JG cell and the renin and pro-renin they store has not been studied in detail.

Our approach involves cellular, biochemical, immunological, genetic, molecular biological and whole animal physiological approaches in an experimental model of diabetes.

Laboratory web site

 https://www.henryford.com/physician-directory/m/mendez-mariela

Publications

 For a complete list of Dr. Mendez's publications, click here

Education

Ph.D. in Pharmacology, National University of Buenos Aires, School of Medicine (2005)
M.S. in Biochemistry. University of Cordoba, Argentina (1998)

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