Michael Kashgarian, MD, FASN
Research & Publications
Biography
News
Locations
Extensive Research Description
Research in my laboratory was directed in three main investigative areas. We study the structural and functional characteristics of transporting epithelia, in particular the cellular mechanisms involved in adaptive changes in response to steroid hormones and changes in the external ionic milieu. The second area of investigation is of the mechanisms involved in the recovery from acute renal failure. These studies concentrate on the contribution of the cytoskeleton to the reorganization of the micro domain distribution of Na,K-ATPase as well as investigating the role of the synthesis and recycling of integral membrane proteins and the contribution of heat shock proteins in this process. Finally, we are also investigating the factors involved in the initiation and progression of glomerulus scarring by defining the pathogenetically relevant parameters of progressive glomerular injury.
My clinical research has focused on the immuopathology of lupus nephritis and in the pathogenesis of acute kidney injury.
Renal Disease, renal transport and ischemia, heat shock proteins, diabetic nephropathy, lupus nephritis, acute kidney injury, Electron Microscopy of tumors; juvenile diabetes. Cellular disruption and restitution. Diabetes.
Coauthors
Research Interests
Cells; Epithelial Cells; Disorders of Environmental Origin; Kidney; Kidney Glomerulus; Kidney Tubules; Lupus Nephritis; Mixed Connective Tissue Disease; Nephrons; Scleroderma, Systemic; Podocytes; Systemic Vasculitis
Selected Publications
- A novel form of human mendelian hypertension featuring nonglucocorticoid-remediable aldosteronism.Geller DS, Zhang J, Wisgerhof MV, Shackleton C, Kashgarian M, Lifton RP. A novel form of human mendelian hypertension featuring nonglucocorticoid-remediable aldosteronism. The Journal Of Clinical Endocrinology And Metabolism 2008, 93: 3117-23. PMID: 18505761, PMCID: PMC2515083, DOI: 10.1210/jc.2008-0594.
- Disruption of Myosin 1e promotes podocyte injury.Krendel M, Kim SV, Willinger T, Wang T, Kashgarian M, Flavell RA, Mooseker MS. Disruption of Myosin 1e promotes podocyte injury. Journal Of The American Society Of Nephrology : JASN 2009, 20: 86-94. PMID: 19005011, PMCID: PMC2615733, DOI: 10.1681/ASN.2007111172.
- Altered renal proximal tubular endocytosis and histology in mice lacking myosin-VI.Gotoh N, Yan Q, Du Z, Biemesderfer D, Kashgarian M, Mooseker MS, Wang T. Altered renal proximal tubular endocytosis and histology in mice lacking myosin-VI. Cytoskeleton (Hoboken, N.J.) 2010, 67: 178-92. PMID: 20175219, PMCID: PMC3468331, DOI: 10.1002/cm.20435.
- Dendritic cells in lupus are not required for activation of T and B cells but promote their expansion, resulting in tissue damage.Teichmann LL, Ols ML, Kashgarian M, Reizis B, Kaplan DH, Shlomchik MJ. Dendritic cells in lupus are not required for activation of T and B cells but promote their expansion, resulting in tissue damage. Immunity 2010, 33: 967-78. PMID: 21167752, PMCID: PMC3010763, DOI: 10.1016/j.immuni.2010.11.025.
- A small-molecule macrophage migration inhibitory factor antagonist protects against glomerulonephritis in lupus-prone NZB/NZW F1 and MRL/lpr mice.Leng L, Chen L, Fan J, Greven D, Arjona A, Du X, Austin D, Kashgarian M, Yin Z, Huang XR, Lan HY, Lolis E, Nikolic-Paterson D, Bucala R. A small-molecule macrophage migration inhibitory factor antagonist protects against glomerulonephritis in lupus-prone NZB/NZW F1 and MRL/lpr mice. Journal Of Immunology (Baltimore, Md. : 1950) 2011, 186: 527-38. PMID: 21106847, PMCID: PMC3124407, DOI: 10.4049/jimmunol.1001767.
- The maximal cytoprotective function of the heat shock protein 27 is dependent on heat shock protein 70.Sreedharan R, Riordan M, Thullin G, Van Why S, Siegel NJ, Kashgarian M. The maximal cytoprotective function of the heat shock protein 27 is dependent on heat shock protein 70. Biochimica Et Biophysica Acta 2011, 1813: 129-35. PMID: 20934464, PMCID: PMC3014454, DOI: 10.1016/j.bbamcr.2010.08.012.