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June 2014 Researcher of Month - Md Khursheed, PhD

Md Khursheed, PhDCurrent Research
Foot ulceration after ischemia and leg amputation is a major post diabetic complication. Impaired angiogenesis after ischemia is the principal cause for this problem.  Therefore, understanding the underlying mechanism of impaired angiogenesis in chronic hyperglycaemic condition is necessary to develop an efficient therapeutic target for its prevention or to reverse this effect in the diabetic population.  Various laboratories including the Diabetes Research Program are trying to understand the underlying mechanism of this deficient angiogenesis.

Previously, our lab identified the central role of the receptor of advanced glycation end products (RAGE) in various diabetic complications including ischemia. The lab developed diabetic mice models for ischemia (using femoral artery ligation) in RAGE-/- and wild-type mice and has shown to have improved angiogenesis in RAGE-/- background.

Importantly, interaction of RAGE with its ligands has been shown to induce expression of pro-inflammatory genes such as CCL2. I am trying to understand the role of various inflammatory signaling mechanisms involved in angiogenesis using in vitro cell culture models derived from wild-type and RAGE-/- diabetic and non-diabetic mice.

Publications
1.  Md Khursheed and Bashyam MD. Apico-basal polarity complex and cancer. J. Biosci. 39(1), March 2014, 145–155.

2.  Md Khursheed, Kolla JN, Kotapalli V, Gupta N, Gowrishankar S, Uppin SG, Sastry R, Koganti S, Sundaram C, Pollack JR, Bashyam MD. ARID1B, a member of the human SWI/SNF chromatin remodeling complex, exhibits tumor suppressor activities in pancreatic cancer cell lines. British Journal of Cancer, 2013, 108:2056-2062.

* Thesis titled: “Identification and functional characterization of novel pancreatic cancer gene(s)” published in University Grants Commission (UGC), Govt. of India national research thesis database “Shodhganga”. http://shodhganga.inflibnet.ac.in/handle/10603/11669

Future Plans

  • My specific aim in this laboratory is to understand deregulated pro-inflammatory signaling mechanism in deficient angiogenesis in chronic hyperglycaemia.
  • My long term goal is to identify the key molecule of deregulated signaling pathway and develop an efficient therapeutic target for this complication.