OMB No. 0925-0001/0002 (Rev. 08/12 Approved Through 8/31/2015)
BIOGRAPHICAL SKETCH
Provide the following information for the Senior/key personnel and other significant contributors.
Follow this format for each person. DO NOT EXCEED FIVE PAGES.
NAME: Mallikarjuna R. Pabbidi, DVM., PhD
eRA COMMONS USER NAME (credential, e.g., agency login): mpabbidi
POSITION TITLE: Assistant Professor of Pharmacology
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as
nursing, include postdoctoral training and residency training if applicable. Add/delete rows as necessary.)
INSTITUTION AND LOCATION
CVSc, Tirupati, AP, India.
SIU-SOM, Springfield, IL, USA.
LUMC, Maywood, IL, USA.
DEGREE
(if applicable)
DVM
Ph.D.
Post-doctoral
Completion
Date
MM/YYYY
12/2000
12/2007
07/2010
FIELD OF STUDY
Veterinary science
Pharmacology
Physiology
A. Personal Statement
My research focus involves studying the role of ion-channels such as potassium, calcium and TRP
channels and their regulation by signaling molecules in the physiological and pathological setting. My
research will yield in identification and discovery of molecular targets that can be modulated
pharmacologically better the health in disease states such as stroke, hypertension, diabetes and vascular
disease. My lab primarily works on 4 questions. (1) How do genes regulate cerebral vascular contraction?
Animal models and expression system will be used to identify mutated genes and their regulation of ionchannels to discover their role in impaired vascular contraction. (2) How does females and estrogen
influence the ion-channels in vascular contraction? We will use male and female rats to study the
influence of sex hormones on vascular contraction. (3) How do resistance vessels such as middle
cerebral arteries differ from conductive vessels such as carotid or aorta in their expression and function of
proteins? We will isolate both types of vessels to measure vascular contraction in response to stretch or
agonists. We will correlate these findings at the molecular level by studying ion-channels function and
quantify these proteins by using western blot or imaging studies. My role on these projects is to perform,
train and supervise the researchers, students and fellows in my laboratory. I have been collaborating with
Dr Roman for the last 3 years and have a well - equipped lab for patch clamp studies both at the wholecell and single channel level. I have over 10 years’ experience in this area. I was trained in
electrophysiology at the Southern Illinois University and my doctoral studies focused on the role of TRP
(Transient Receptor potential) channels in diabetic neuropathy. As a postdoctoral fellow at the Loyola
University, I obtained further training in cardiac electrophysiology and expanded my technical capabilities.
In the last 3 years I have focused on the control of renal, cerebral and pulmonary vascular tone using
patch clamp techniques, vascular reactivity and have over 14 papers in high impact journals that
document my experience in this area.
1. Reddy M. Pabbidi, Shuang-Quan Yu, Siying Peng, Romesh Khardori, Mary E. Pauza, and Louis S.
Premkumar. Influence of TRPV1 on diabetes-induced alterations in thermal pain sensitivity. Mol Pain.
2008 4:9 doi: 10.1186/1744-8069-4-9: Highly accessed article.
2. Pabbidi MR, Ji X, Wang YG, Samarel AM, Lipsius SL. Cell Attachment to Laminin Enhances β2Adrenergic Receptor Stimulation of L-type Ca2+ Current via Activation of Cytosolic Phospholipase A 2
Signalling in Cat Atrial Myocytes. J Physiol. 2009 Oct 15; 587 (Pt 20):4785-97. Epub 2009 Aug 24.
3. Pabbidi MR, Mazur O, Fan F, Farley JM, Gebremedhin D, Harder DR, Roman RJ. Enhanced large
conductance K+ channel (BK) activity contributes to the impaired myogenic response in the cerebral
vasculature of Fawn Hooded Hypertensive rats. Am J Physiol Heart Circ Physiol. 2014 Apr
B. Positions and Honors
Positions and Employment
2001 – 2003
Trainee Veterinarian, DRL, Discovery Research Foundation, India.
2007 – 2010
Res-Associate of Physiology, Loyola University Medical Center, IL.
2010 – 2012
Instructor of Pharmacology, UMMC, Jackson, MS.
2013 – Present Assistant Professor of Pharmacology, UMMC, Jackson, MS.
Other Experience and Professional Memberships
2004 – Past Member of Society for Neuroscience.
2009 – Past Member of Biophysical society.
2010 – Present Member of EB (Experimental Biology)
2012 – Present Member of AHA (American Heart Association)
Honors
2004 –Participation certificate for oral presentation in combined research symposium Illinois, USA.
2005 –Participation certificate for oral presentation combined research symposium Illinois, USA.
2006 –Participation and survival certificate for 10 day course in CSHL, NY, USA.
2012 –Annual High Blood Pressure Research Conference. New Investigator Award, AHA 2012.
C. Contribution to Science
Hypertension and diabetes are the major risk factors for stroke and blood pressure is not adequately
controlled in more than 40% of the hypertensive patients. Impaired myogenic control of cerebral blood
flow (CBF) is observed in hypertension and diabetes, and is predictive of neurologic deterioration in
patients with these conditions. Our studies utilizing rodents identify mutation in adducin genes that
contributes to end organ damage by impairment of vascular function and is associated with increased K +
channel function. This information could be used for developing genetic tests to identify susceptible
hypertensive patients. This information could also lead to the discovery of BK or PKC or adducin
modulators that can restore vascular function in hypertensive individuals exhibiting adducin mutations and
possibly lessen the risk of stroke and end organ damage in hypertensive and diabetic patients.
a. Pabbidi MR, Mazur O, Fan F, Farley JM, Gebremedhin D, Harder DR, Roman RJ. Enhanced
large conductance K+ channel (BK) activity contributes to the impaired myogenic response in
the cerebral vasculature of Fawn Hooded Hypertensive rats. Am J Physiol Heart Circ Physiol.
2014 Apr 1;306(7):H989-H1000. doi:0.1152/ ajpheart. 00636 .2013.Epub 2014 Jan 24.
b. Pabbidi MR, Juncos JP, Juncos LA, Renic M, Tullos H, Lazar J, Jacob HJ, Harder DR,
Roman RJ. Identification of a region of rat chromosome 1 that impairs the myogenic
response and autoregulation of cerebral blood flow in Fawn Hooded Hypertensive rats. Am J
Physiol Heart Circ Physiol. 2013 Jan; 304(2):H311-7. PMID: 23144316.
In addition to the contributions described above, under the guidance of Dr. Lipsius at Loyola (2008 to
2010) we identified a signaling pathway that cardiac cells change to during adaptation to hypertrophic
stimuli. We found that the increase in extracellular matrix such as laminin can enhance beta 2 adrenergic
signaling via activation of phospholipase A2. Through this adaptation, heart counteracts the impaired
function. These studies emphasized on altered cellular signaling in the context of cardiac hypertrophy.
c. Pabbidi MR, Ji X, Wang YG, Samarel AM, Lipsius SL. Cell Attachment to Laminin Enhances
β2-Adrenergic Receptor Stimulation of L-type Ca2+ Current via Activation of Cytosolic
Phospholipase A2 Signalling in Cat Atrial Myocytes. J Physiol. 2009 Oct 15; 587 (Pt 20):478597. Epub 2009 Aug 24.
d. Wang YG, Ji X, Pabbidi MR, Samarel AM, Lipsius SL. Laminin Acts via FAK/PI-(3) K/Akt to
Down-Regulate (beta) 1-Adrenergic Receptor Signalling in Cat Atrial Myocytes. J Physiol.
2009 Feb 1; 587(Pt 3):541-50. Epub 2008 Dec 8.
My early publications (2004-2007) directly addressed the fact that diabetic peripheral neuropathy (DPN) is
characterized by both high (hyperalgesia) and low pain (hypoalgesia) sensitivity in streptozotocin (STZ)–
induced diabetes. This altered pain sensitivity correlates with expression and function of TRPV1
(Transient receptor potential vanilloid) channel that is activated by ingredient in capsicum called
capsaicin. By providing this evidence, our studies changed the way capsaicin is used in DPN. Our
findings also led to an accidental discovery that STZ it self can contribute to hyperalgesia and advice
scientific community to exercise caution in interpreting pain sensitivity in STZ-induced diabetic models.
Our work also suggests that RTX (resiniferatoxin), a toxin present in cactus plant can open TRPV1
channel for longer durations and is ideal for chronic pain condition. I served as the primary investigator or
co-investigator in all of these studies.
a. Reddy M Pabbidi, De-Shou Cao, Arti Parihar, Mary E Pauza, and S. Louis Premkumar.
Direct Role of Streptozotocin in Inducing Thermal Hyperalgesia by Enhanced Expression of
TRPV1 in Sensory Neurons. Mol. Pharmacol. 2008 73: 995-1004.
b. Reddy M. Pabbidi, Shuang-Quan Yu, Siying Peng, Romesh Khardori, Mary E. Pauza, and
Louis S. Premkumar. Influence of TRPV1 on diabetes-induced alterations in thermal pain
sensitivity. Mol Pain. 2008 4:9 doi: 10.1186/1744-8069-4-9: Highly accessed article.
c. Manish Raisinghani, Reddy M Pabbidi and Louis S Premkumar. 2005. Activation of
transient receptor potential vanilloid 1 (TRPV1) by resiniferatoxin. J Physiol 567.3 pp 771786.
Complete List of Published Work in My Bibliography:
http://www.ncbi.nlm.nih.gov/sites/myncbi/1H9qitv6vpg51/bibliography/40986242/public/?sort=date&directi
on=descending
D. Research Support
Ongoing Research Support
1R01DK104184-01
Roman (PI)
10/01/14-09/30/19
Renal microcirculation and hypertension induced renal injury
The goal of this study is to identify and study the genes responsible for impaired myogenic response in
FHH rats.
Role: Co-Investigator
13SDG14000006
Pabbidi
01/01/13-03/30/16
Genetic basis of cerebral blood flow (CBF) autoregulation in FHH rats.
The goal of this study is to identify and study the genes responsible for impaired myogenic response in
FHH rats.
Role: PI
Completed Research Support
IRSP, UMMC
Pabbidi
01/01/11-03/30/12
Genetic basis of cerebral blood flow (CBF) autoregulation in FHH rats.
The goal of this study is to identify and study the genes responsible for impaired myogenic response in
FHH rats.
Role: PI