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Rao N. Jaladanki, PhD

Academic Title:

Associate Professor

Primary Appointment:

Surgery

Additional Title:

Research Health Scientist, VA Maryland Health Care System

Location:

VAMC, 10 N. Greene Street

Phone (Primary):

(410) 605-7808

Fax:

(410) 605-7949

Education and Training

Dr. Jaladanki received his doctorate degree in 1992 from Sri Venkateswara University, India. After completing Ph.D. degree, he joined as a Rockefeller Foundation Post-Doctoral Research Fellow in the Department of Physiology, Southern Illinois University, Carbondale, IL and worked in the field of endocrinology during 1993-95. This postdoctoral work formed the foundation for Dr. Jaladanki to pursue the future research on the role of hormones related to Gastrointestinal Physiology. In 1997, he joined the Department of Surgery at University of Maryland School of Medicine and worked in GI research laboratories. His research examined the polyamine mediated GI growth, proliferation, and mucosal restitution signaling pathways. He was later promoted to the rank of Assistant Professor in the Department of Surgery in 2004, and to Associate Professor level in 2015.

Research/Clinical Keywords

Gut Mucosal growth, cell proliferation, Mucosal Restitution, GI injury and healing, microRNAs, Posttranscriptional Regulation

Highlighted Publications

1.       Rathor N, Zhuang R, Wang J-Y, Donahue JM,Turner DJ and Rao JN.  Src-mediated Caveolin-1 regulates intestinal epithelial restitution by altering Ca2+ influx after             wounding.  Am J Physiol Gastrointest and Liver Physiol, 306:  G650-G658, 2014.

2.       Rathor N, Chung HK, Wang SR, Wang J-Y, Turner DJ and Rao JN.  Caveolin-1 enhances rapid mucosal restitution by activating TRPC1-mediated Ca2+ signaling.               Physiol Rep  2: e12193, 2014.

3.       Liu L, Christodoulou E, Rao JN, Zou T, Xiao L, Chung HK, Yang H, Gorospe M, Kontoyiannis D,  and Wang J-Y. RNA-binding protein HuR promotes growth of small             intestinal mucosa by activating the Wnt signaling pathway.  Mol Biol Cell  25: 3308-3318, 2014.

4.       Zou T, Rao JN, Liu L, Xiao L, Chung HK, Li Y, Chen G, Gorospe M,  and Wang J-Y. JunD enhances miR-29b levels transcriptionally and post-transcriptionally to                   inhibit proliferation of intestinal epithelial cells.  Am J Physiol Cell Physiol308: C813-C824, 2015.

5.       Chung HK, Rathor N, Wang SR, Wang J-Y, and Rao JN.  RhoA enhances store-operated Ca2+ entry and intestinal epithelial restitution by interacting with TRPC1               after wounding.  Am J Physiol Gastrointest and Liver Physiol, 309:  G759-G767, 2015.

6.       Xiao L, Rao JN, Cao S, Liu L, Chung HK, Zhang Y, Zhang J, Liu Y, Gorospe M, and Wang J-Y.  Long noncoding RNA SPRY4-IT1 regulates intestinal epithelial barrier             function by modulating the expression levels of tight junction proteins.  Mol Biol Cell, 27: 617-626, 2016.

7.       Li Y, Chen G, Wang J, Zou T, Liu L, Xiao L,Chung HK, Rao JN, and Wang J-Y.  Posttranscriptional regulation of Wnt-coreceptor LRP6 and RNA-bindg protein HuR by           miR-29b in intestinal epithelial cells.  Biochem J, 473: 1641-1649, 2016.

8.       Hansraj NZ, Xiao L, Wu J, Chen G, Turner DJ, Wang J-Y, and Rao JN.  Posttranscriptional regulation of 14-3-3z by RNA-binding protein HuR modulating intestinal               epithelial restitution after wounding.  Physiol Rep  4: e12858, 2016.

9.       Liu L, Zhuang R, Xiao L, Chung HK, Luo J, Turner DJ, Rao JN, Gorospe M, and Wang J-Y.  HuR Enhances Early Restitution of the Intestinal Epithelium by Increasing           Cdc42 Translation.  Mol Cell Biol, 2016 Dec 28. pii: MCB.00574-16. doi: 10.1128/MCB.00574-16. [Epub ahead of print].

10.     Wang PY, Wang SR, Xiao L, Chen J, Wang J-Yand Rao JN.  c-Jun Enhances Intestinal Epithelial Restitution after Wounding by Increasing Phospholipase C-γ1                     Transcription.    Am J Physiol Cell Physiol, 2017 Jan 18. doi: 10.1152/ajpcell.00330.2016. [Epub ahead of print].

Additional Publication Citations

https://www.ncbi.nlm.nih.gov/sites/myncbi/1FoEh-V_G1B5K/bibliography/41493572/public/?sort=date&direction=descending

Research Interests

My research is intended to elucidate the mechanistic roles of Ca2+-permeable channels in the regulation of intestinal epithelial restitution after wounding and their regulation by cellular polyamines. Continuing along these lines, our group has performed cell imaging/MS-2 system to localize specific mRNA subcellular distribution and mRNA traffic into/out from processing-body/stress granules during restitution and has defined the involvement of RNA-binding proteins and microRNAs in the regulation of acute mucosal injury and repair. Our team also has developed innovative experimental approaches that utilize the difference between multiple methods and stimulus modalities to infer underlying mechanisms of gut mucosal injury/repair and barrier dysfunction. The data generated also strengthens our long-term goal to develop therapeutic approaches for GI mucosal injury-related diseases and to maintain epithelial integrity under various critical surgical conditions.  

Clinical Specialty Details

N/A

Awards and Affiliations

Dr. Jaladanki has also been actively involved in basic surgical research teaching in Cell Biology Group over the past several years. He instructs young research fellows, surgical residents, medical students, and college students at the lab and serves as a co-mentor for college students during the period of summer research. He is also involved with various Baltimore VAMC and UMB institutional committees. Dr. Jaladanki has also been an active member in scientific societies, including American Gastroenterology Association and American Physiological Society.

Grants and Contracts

Department of Veterans Affairs MERIT Award

Lab Techniques and Equipment

Lab Techniques and Equipment

• Gut mucosal injury models in vitro and in vivo
• small GTP binding proteins, GPCRs during wound healing
• Measurements of paracellular permeability and barrier functions
• microRNAs regulation on gut mucosal integrity
• RNA-pull down assays

• Polysome profile analysis
• Transient (adenoviral system) and stable gene transfection
• Promoter deletion, exchange, and point mutations and reporter gene assays
• Fluorescence measurement of intracellular Ca2+ concentration

• miRNA profiles and RNA Binding Proteins