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Khamaisi Mogher, M.D. Ph.D

Assistant Professor

MD, 2003- Ben-Gurion University, Beer-Sheva
Ph.D, 2002- Ben-Gurion University, Beer-Sheva

Exploring the mechanisms for impaired wound healing in diabetes

Chronic foot ulcers are one of the most common and serious complications of diabetes, resulting in more than 2,000 amputations per year in Israel alone. My research is aimed at exploring the molecular mechanisms involved in impaired wound healing in long standing diabetes. To that end we use combined in vivo and in vitro studies, as well as human stem cells and other differentiated cells. We recently reported that persistent Protein Kinase C -δ (PKCδ) elevations in fibroblasts from diabetic patients inhibits insulin signaling which results in impaired wound healing, pointing to PKCδ inhibition as a potential therapy for improved wound healing in diabetic patients.
One of our ongoing projects involves the finding that a novel microRNA (miRNA) modulates PKCδ expression in diabetes and affects wound healing capacity. This suggests a potential role for this miRNA in regulating PKC expression in diabetic wounds, possibly shedding light on novel disease mechanisms with potential implications to treatment strategies. 


Representative publications


1. Khamaisi M, Keenan H, Katagiri S, Park K, Li Q, Yasutaka M, Qi W, Rask- Madsen C, Orgill DP, Huang C, King GL:  Persistent activation of PKC and inhibition of insulin actions in fibroblasts from type 1 diabetes with CVD impaired wound healing.  J Clin Invest 126(3):837-53, 2016.

2. Bhatt S, Gupta MK, Khamaisi M, Martinez R, Gritsenko MA, Wagner BK, Guy Pe, Busskamp V, Takatani T, Wu G, El Ouaamari A, Dirice E, Liew CW, Keenan HA, Smith RD, Church G, Wagers AJ, Weiss R, Qian WJ, King GL, Kulkarni RN: Preserved DNA Repair Pathway Protects From Complications in Long-standing Type 1 Diabetes. Cell Metabolism 4;22(2):239-52, 2015.

3. Khamaisi M, Toukan H, Axelrod JH, Rosenberger C, Skarzinski G, Shina A, Meidan R, Koesters R, Rosen S, Walkinshaw G, Mimura I, Nangaku M, Heyman SN:  Endothelin-converting enzyme is a plausible target gene for hypoxia-inducible factor.  Kidney Int 87(4):761-70, 2015.

4. Molcho S, Peer A, Berg T, Futerman B, Khamaisi M: Diabetes Microvascular Disease and the Risk for bisphosphonate-related Osteonecrosis of the Jaw: A Single Center Study. J Clin Endocrinol Metab 98(11):E1807-12, 2013.

5. Khamaisi M, Skarzinski G, Mekler J, Farid A, Shay S, Damouni R, Ariel I, Bursztyn M: Hyperinsuline- mia increased placenta Endothelin Converting Enzyme-1 expression in trophoblasts. Am J Hypertens 25(1):109-14, 2012.

Figure Legend

Knockdown of PKCδ in Medalist fibroblasts improves wound healing when transplanted into a diabetic host. Macroscopic wound area surfaces not covered by an epithelial layer (A) and H&E-stained sections for open wound area and granulation tissues on day 9 after initial wounding (B) in control fibroblasts infected with Ad-GFP or diabetic fibroblasts infected with Ad-GFP or Ad-dnPKCδ. Percentage of the open wound areas (C) and VEGF mRNA in granulation tissues (D) on day 9 after wounding in the different treatment groups. Data represent the mean ± SD. n = 7 for the control fibroblast group; n = 8 for the diabetic group. The criteria for selecting the cell lines for these experiments were completely random, and the clinical and demographic characteristics of the selected subjects did not differ from those of the rest of the patients. Scale bars: 50 μm.

Email: m_khamaisi@rambam.health.gov.il
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