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Novel studies identify small RNAs connecting inflammation and obesity
Obesity, a prevalent threat among one-third of the adult
population in the United States, is associated with cardiovascular
disease and metabolic disorders such as diabetes. A major
contributor to this danger is inflamed adipose tissue, or body
fat. A recent study by a team at the Texas A&M College of
Veterinary Medicine & Biomedical Sciences (CVM) indicates that
small RNAs, or microRNAs (miRNAs), which are part of a person's
genetic code, can guide inflammatory or anti-inflammatory action of
macrophages - a special type of cell - in the adipose tissue that
are crucial for our immune defense and important regulators once
permeated into tissues. The study, led by Dr. Beiyan Zhou,
assistant professor of physiology and pharmacology at the CVM, was
recently accepted for publication by Circulation, the leading
journal of the American Heart Association (AHA).
Macrophages are a type of immune cell which often responds to
infections or wound repairings. Zhou said the study focuses
on understanding how microRNA influences these cells when
regulating the "good" and "bad" fat cells.
Cong Meng, a graduate student in Zhou's laboratory and the
co-first author of the article, said adipose tissue
infiltrated by macrophages can be polarized to M1,"bad," and
Zhou said macrophages in fat tissues act in a protective,
anti-inflammatory role in people who are not obese. For those
that are obese, or have plaque on their blood-vessel walls,
macrophages infiltrate the tissues, try to correct the problem, and
"Both M1 and M2 macrophages are regulators in atherosclerotic
lesions that play a critical role in the development of
cardiovascular diseases. One miRNA can regulate many genes
simultaneously. By harnessing one-crucial miRNA, you can shift the
network to either direction: inflammatory or anti-inflammatory,"
said Guoqing Zhuang, the co-first author for this study and
postdoctoral fellow in Zhou's lab.
Xin Guo, a graduate student in Assistant Professor Chaodong Wu's
laboratory in the Department of Nutrition and Food Sciences at
Texas A&M College of Agriculture and Life Sciences, validated
the adipose tissue signaling pathways.
"In this study, we demonstrated that miR-223 is a novel and
crucial regulator of macrophage polarization and is indicated for
suppressing pro-inflammatory and enhancing anti-inflammatory
responses," Guo said.
Dr. Stephen Safe, collaborator on the study and professor at the
CVM, said the results hold great promise in the development of
treatments for metabolic disorders.
"This study has identified a new microRNA-based paradigm for
regulation of insulin sensitivity," Safe said. "The results may
ultimately provide the basis for using microRNA analogs or
chemicals for microRNA regulated genes to treat insulin
resistance-related diseases," he added.
While this study represents a starting point in developing new
therapeutic drugs for diabetes, Dr. Robert Chapkin, collaborator on
the study and a Regent Professor in the Department of Nutrition and
Food Sciences, explained there is currently a need for new drugs
since most are no longer sold due to severe side effects.
"Their highly novel finding suggests that because macrophages
play an important role in mediating metabolic disorders including
obesity-induced insulin resistance, that microRNA-223 may be a
metabolic target for therapies designed to regulate systemic
inflammation and energy metabolism," he added.
The paper sparked positive feedback from the science community
including an editorial introduction (published on the same issue of
Circulation) by Dr. Jiandie Lin from the University of
"Previous studies have implicated different miRNA members in the
regulations of innate and adaptive immune responses as well as
immune cell differentiation," Lin said. "However, a role for miRNA
in macrophage polarization has not been explored and this research
is the first one to link macrophage function and obesity related
Angela G. Clendenin
Director, Communications & Public Relations
Ofc - (979) 862-2675
Cell - (979) 739-5718
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