Mohammed S. Razzaque, MD, PhD.
Instructor
Department of Developmental Biology
Office: REB 304
188 Longwood Ave.
Boston, MA 02115
Telephone: (617) 432-5768 
FAX (617) 432-5767
Email: mrazzaque@hms.harvard.edu  

My laboratory studies mechanisms of wound healing and matrix remodeling, systemic regulation of mineral ion homeostasis, and molecular events of premature ageing that affect survival.

1. In the wound healing project, in collaboration with Prof. Taguchi of Nagasaki University, Japan, we are studying to identify factors that initiate and propagate organ-specific fibrosis. We are particularly interested in heat shock protein 47 (HSP47) that controls procollagen assembly and processing. We found a close association between increased activity of HSP47 and excessive accumulation of collagens in organ fibrosis. More importantly, suppressing the activities of HSP47 by genetic manipulation can reduce progression of fibrosis in various experimental models. Currently we are interested in studying the in vivo pharmacological effects of small molecule inhibitors for HSP47 in delaying the progression of fibrotic diseases in various organ systems.

2. In the systemic regulation of mineral ion homeostasis project, in collaboration with Dr. Lanske, we are investigating the molecular basis for physiological regulation of calcium and phosphate homeostasis, using mouse genetics as an in vivo tool. Our main interest is to determine how fibroblast growth factor 23 (FGF23), vitamin-D and sodium-phosphate cotransporters coordinately regulate systemic mineral ion homeostasis.

3. In the premature ageing project, we are studying genetic causes of accelerated mammalian ageing. Our in vivo studies involve identification of factors and events that induce premature ageing-like phenotypes in klotho ablated mice. We are also currently working on understanding the molecular basis of increase survival (almost 25%) of transgenic strain of rats in which growth hormone (GH) and insulin-like growth factor 1 (IGF-1) activities are genetically suppressed by in vivo induction of an antisense GH transgene.

Recent Publications:

Razzaque MS.  Can fibroblast growth factor 23 fine-tune therapies for diseases of abnormal mineral ion metabolism? Nature Clinical Practice Endocrinology & Metabolism 2007; 3:788-789.

Goetz R, Beenken A, Ibrahimi OA, Kalinina J, Olsen SK, Eliseenkova AV, Xu C, Neubert T, Zhang F, Linhardt RJ, Yu X, White KE, Inagaki T, Kliewer SA, Yamamoto M, Kurosu H, Ogawa Y, Kuro-O M, Lanske B, Razzaque MS, Mohammadi M. Molecular insights into the klotho-dependent, endocrine mode of action of FGF19 subfamily members. Molecular Cellular Biology 2007; 27:3417-28.

Taguchi T, Razzaque MS.  The collagen-specific molecular chaperone HSP47: is there a role in fibrosis? Trends in Molecular Medicine 2007; 13:45-53.

Ogawa Y, Razzaque MS, Kameyama K, Hasegawa G, Shimmura S, Kawai M, Okamoto S, Ikeda Y, Tsubota K, Kawakami Y, Kuwana M. Role of heat shock protein 47, a collagen-binding chaperone, in lacrimal gland disese in patients with cGVHD. Investigation Ophthalmology & Visual Science 2007; 48:1079-1086.

Lanske B, Razzaque MS.  Mineral ion metabolism and aging: the Fgf-23 enigma. Current Opinion in Nephrology & Hypertension 2007; 16:311-318.

Razzaque MS.  Does renal ageing affect survival? Ageing Research Review 2007; 6:211-22.

Sitara D, Razzaque MS, St-Arnaud R, Taguchi T, Erben RG, Lanske B.  Ablation of vitamin D activation pathway rescues anomalies in Fgf-23 null animals.  American Journal of Pathology 2006: 169:2161-70.

Razzaque MS, Lanske B. Hypervitaminosis D and premature aging: lessons learned from Fgf-23 and klotho mutant mice. Trends in Molecular Medicine 2006; 12:298-305.

Razzaque MS, Sitara D, Taguchi T, St-Arnaud R, Lanske B. Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process. FASEB Journal. 2006; 20:720-2

Zha Y, Le VT, Higami Y, Shimokawa I, Taguchi T, Razzaque MS.  Life-long suppression of growth hormone-insulin-like growth factor-1 activity in genetically altered rats could prevent age-related renal damage. Endocrinology 2006 147: 5690-5698.