Chand, Hitendra Singh
Title: Associate Professor
Office: AHC1 418C
Dr. Chand received his PhD from the University of Delhi, India and got his postdoctoral training at the Department of Pathology, UNM Health Science Center, Albuquerque, NM. As an Assistant Professor at Center for Infectious Diseases and Immunology (CIDI), UNM School of Medicine, Dr. Chand worked on systems-based biology to study the opportunistic pulmonary infectious diseases and allergic asthma. He pursued his interest in respiratory biology at Lovelace Respiratory Research Institute (LRRI), Albuquerque, NM, and investigated the molecular mechanisms involved in programmed cell death and inflammation using the experimental animal models of airway diseases. Currently, Dr. Chand is serving as an Associate Professor (tenure-track) in the Department of Immunology and the Center for Personalized Nanomedicine at Florida International University.
Dr. Chand’s primary research interest involves understanding the mechanisms of airway inflammation and remodeling in chronic airway diseases by specifically focusing on mucous hypersecretion pathways. The projects employ cellular, molecular, and animal model approaches to investigate the role of inflammatory mediators in airway remodeling. The inhalational exposure to various toxicants and allergens causes airway epithelial cells to engage adaptive and cytoprotective pathways. One such mechanism is epithelial cell extrusion whereby dying or unwanted cells are removed while preserving the barrier integrity. And either infrequent or frequent extrusion could occlude the lung function. In certain susceptible population these pathways are dysregulated leading to aberrant mucous production as observed in patients with allergic asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD).
Current projects include:
- Investigating the mechanisms of mucous cell survival/death pathways
- Role of epithelial cell extrusion in chronic airway diseases
- Role of HIV-1 infection and substance abuse in chronic diseases
- Targeting chronic diseases with nanotechnology - Inhalational Nano-delivery
- Jang JH#, Chand HS#, Bruse S, Doyle-Eisele M, Royer C, McDonald J, Qualls C, Klingelhutz AJ, Lin Y, Mallampalli R, Tesfaigzi Y, Nyunoya T. "Connective Tissue Growth Factor Promotes Pulmonary Epithelial Cell Senescence and is Associated with COPD Severity." COPD (In Press), (#Equal contribution).
- Chand HS, Mebratu YA, Montera M, Tesfaigzi Y. “T cells Suppress Memory- Dependent Rapid Mucous Cell Metaplasia in Mouse Airways.” Respiratory Research 2016, 17:132.
- Jang JH, Lee JH, Chand HS, Lee JS, Lin Y, Weathington N, Mallampalli R, Jeon YJ, Nyunoya T. “APO-9'-Fucoxanthinone extracted from Undariopsis peteseniana protects oxidative stress-mediated apoptosis in cigarette smoke-exposed human airway epithelial cells.” Mar. Drugs 2016 Jul 21;14(7).
- Mebratu YA, Tipper J, Chand HS, Walton S, Harrod KS, Tesfaigzi Y. “Bik Mediates Caspase-Dependent Cleavage of Viral Proteins to Promote Influenza A Virus Infection.” Am. J. Respir. Cell. Mol. Biol. 2016 May;54(5):664-73.
- Singh SP, Chand HS, et al., “HIF-1α Plays a Critical Role in the Gestational Sidestream Smoke-Induced Bronchopulmonary Dysplasia in Mice.” PLOS One 2015 10(9): e0137757.
- WuZ,HuCA,WuG,ZhaorigetuS,ChandH,et.al.,"Intimacyandadeadlyfeud:the interplay of autophagy and apoptosis mediated by amino acids." Amino Acids 2015. 47(10):2089-99.
- Awji EG, Chand HS, Bruse S, Smith KR, Colby JK, Mebratu Y, Levy BD, Tesfaigzi Y. “Wood Smoke Enhances Cigarette Smoke-Induced Inflammation by Inducing the Aryl Hydrocarbon Receptor Repressor in Airway Epithelial Cells.” Am. J. Respir. Cell. Mol. Biol. 2015 Mar; 52(3): 377-86.
- ChandHS,MontanoG,HuangX,RandellSC,PetersenH,andTesfaigziY.“Avariant in the proline-rich domain of p53 restricts the mucus secretory phenotype by regulating SPDEF and Bcl-2 expression.” Nature Communications 2014. Nov 27; 5:5567.
- Nyunoya T, Mebratu Y, Contreras A, Delgado-Vargas M, Chand HS and Tesfaigzi Y: “Molecular Processes that Drive Cigarette Smoke-Induced Effects on Epithelial Cells of the Lung.” Am. J. Resp. Cell Mol. Biol. 2014; 50(3):471-82.
- Contreras AU, Mebratu Y, Hu CA, Ryter SW, Choi AMK, Lin Y, Xiang J, Chand H, and Tesfaigzi Y. “Deacetylation of p53 Induces Autophagy by Suppressing Bmf Expression.” J. Cell Biol. 2013; 201:427-437.
- Singh SP, Gundavarapu S, Smith KR, Chand HS, et al. “Gestational Exposure of Mice to Secondhand Cigarette Smoke Causes Bronchopulmonary Dysplasia Blocked by the Nicotinic Receptor Antagonist Mecamylamine.” Environ. Health Perspect. 2013; 121(8):957-64.
- Chand HS, Woldegiorgis Z, Schwalm K, McDonald J and Tesfaigzi Y. “Acute Inflammation Induces IGF-1 to Mediate Bcl-2 and Muc5ac Expression in Airway Epithelial Cells.” Am. J. Resp. Cell Mol. Biol. 2012; 47(6):784-791.
- Chand HS, Harris JF, Mebratu Y, Chen Y, Wright P, Randell SH, Hotchkiss J and Tesfaigzi Y. “Intracellular IGF-I Induces Bcl-2 Expression in Airway Epithelial Cells.” J. Immunol. 2012; 188(9): 4581-4589.
- Chand HS, Schuyler M, Joste N, Hensler C, Tesfaigzi Y, Masten B, Schrader R and Lipscomb MF. “Anti-IgE Therapy Results in Decreased Myeloid Dendritic Cells in Asthmatic Airways.” J Allergy Clin. Immunol. 2010; 125(5):1157-1158.
- Hansen SJ, Rushton J, Dekonenko A, Chand HS, et al., “Cowpox virus inhibits human dendritic cell immune function by nonlethal, nonproductive infection.” Virology. 2011; 412(2):411-425.
- Chand HS, Drysdale M, Lovchik J, Koehler TM, Lipscomb MF, and Lyons CR. “Discriminating virulence mechanisms among Bacillus anthracis strains by using a murine subcutaneous infection model.” Infect Immun. 2009; 77(1):429-5.