Mariela Mendez

projects
Role of the immune system in diabetec kidney disease (ongoing)

Faculty Profile

Asst Professor FTA (Res)
fb5881@wayne.edu

Office Address

Integrative Biosciences Building
iBIO-1413
6435 Woodward, Detroit MI

 

Phone

313-343-2731

Position Title

Assistant Scientist-Hypertension and Vascular Research Division, Henry Ford Hospital
Assistant Professor (FTA)-Department of Physiology, Wayne State University

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

  • NIH/NHLBI FOCUS/PRIDE programs for Advanced Early Stage Investigators. UCSD. La Jolla, California. 2019-2020
  • Travel Award. Gordon Research conference on Angiotensin. Ciocco, Italy. Feb 9-14, 2020.
  • Top 2% abstract graded. American Heart Association. Council of Hypertension. Invited to present at Scientific Sessions 2017
  • NIH-NIDDK RO3. Small Grants for New Investigators to Promote Diversity in Health-Related Research (2015-2019).
  • Winner, top award for scientific merit (cash award), 13th Annual Research Symposium, HFMG Academic Programs, Henry Ford Hospital, April, 2016.
  • Winner, top award for scientific merit (Cash Award). Henry Ford Health System. 12th Annual Research Symposium, HFMG Academic Programs, April, 2015.
  • Young Investigator Symposium Awardee. American Society of Nephrology: Organized by Kidney Council/American Heart Association. 2014
  • Renal Research Recognition Award. Renal Section. Experimental Biology. San Diego, CA, 2014.
  • Minority Travel Award. American Physiological Society- 2013.
  • Winner, top award for scientific merit (cash award), Henry Ford Health System. 10th Annual Research Symposium, 2013.
  • Scientist Development Grant, American Heart Association. National (2013-2017)
  • Young Investigator Travel Award. Kidney Council, American Heart Association. Council of High Blood Pressure. New Orleans 2013.
  • Editorial Board, American Journal of Physiology-Renal Physiology. 2011-Present
  • Caroline tum Suden/Francis A. Hellebrandt Professional Opportunity Award, Committee on Women in Physiology. American Physiological Society. 2011
  • Winner, top award for scientific merit (cash award), Henry Ford Health System 8th Annual Research Symposium, 2011.
  • Finalist, International Society of Hypertension-ISH New Investigators Symposium. Orlando, Florida. 2011
  • Travel award for Professional Development Seminar (PDS). Women in Nephrology. American Society of Nephrology. Denver, CO, 2010.
  • Finalist, Excellence in Renal Research Award for post-doctoral fellows. American Physiological Society. Experimental Biology, 2010.
  • Postdoctoral Fellowship NIH/F32-NRSA, National Institutes of Health. 2009-2012
  • Postdoctoral Fellowship, National Kidney Foundation, January 2008-2009.
  • Winner, top award for scientific merit (cash award), Henry Ford Health System 1st Annual Research Symposium, 2004.
  • Fellowship Grant, American Heart Association/Michigan Affiliate, 2001-2002.

Education

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

Suffix

Ph.D.

Research Description

My laboratory is interested in studying the biology and mechanisms of exocytosis and dysregulation of renin. Renin is the single most important enzyme for blood pressure control since it is the rate limiting step in the production of angiotensin II. Hypertension affects up to 50% of patients with type 1 diabetes (20-25 million in the US) who also develop kidney damage in most cases. The mechanisms by which diabetes causes hypertension are unclear. Renin is expressed in renal Juxtaglomerular Cells (JG cells) as a pro-peptide (pro-renin), where it matures after cleavage of the pro-segment, being stored in secretory granules. Previous studies have hinted to the detrimental involvement of pro-renin in kidney damage in diabetes. The precise mechanisms increasing renin and pro-renin in diabetes are not clear. Moreover, the role of JG cells in this process is unknown.


Our long term goal is to uncover novel targets for development of pharmacological agents to prevent hypertension and kidney damage in diabetes. Our overall objective is to determine the mechanisms of renin and pro-renin release, and their implication in the development of hypertension and kidney damage in a progressive model of type 1 diabetes.

Affiliated Departments

Affiliated Research Units

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