Petit Institute Seminar

Event Details
  • Date/Time:
    • Friday April 19, 2019
      3:00 pm - 4:00 pm
  • Location: Krone Engineered Biosystems Building, Room 1005 - Atlanta, GA
  • Phone:
  • URL:
  • Email:
  • Fee(s):
    N/A
  • Extras:
Contact

Brandon Dixon - faculty host

Summaries

Summary Sentence: “Regulation of Mesenteric Lymphatics in Metabolic Syndrome” - Mariappan Muthuchamy, Ph.D. - Texas A&M College of Medicine

Full Summary: No summary paragraph submitted.

“Regulation of Mesenteric Lymphatics in Metabolic Syndrome”

Mariappan Muthuchamy, Ph.D.
Professor
Medical Physiology
Texas A&M College of Medicine

Lymphatic muscle is uniquely composed of both smooth and striated muscle components and studies elucidating their contractile behavior have unequivocally established that this is a new class of muscle that is distinct from smooth and cardiac/skeletal muscle types. Lymphatic muscle exhibits rapid, phasic contractile activity that drives the intrinsic lymphatic pumping in addition to the slower, tonic form of contractions. One of our goals is to elucidate the contractile regulatory mechanisms of lymphatic muscle in normal and in different inflammation animal models. Insulin resistance is a critical determinant of the onset and progression of several metabolic diseases, such as obesity, metabolic syndrome (MetSyn) and type 2-diabetes. A state of chronic, sub-acute inflammation is believed to be involved in the pathogenesis of insulin resistance and understanding the insulin resistant mechanisms may provide new targets for treatment of MetSyn. Lymphatic function is impaired in a high-fructose diet-induced MetSyn rat model and that is associated with an increase macrophage investiture into, and along, the mesenteric lymphatic collecting vessels. Additionally, insulin resistant lymphatic muscle cells (LMCs) exhibit selective impairment in PI3K/AKT pathway and enhancement in ERK/p38MAPK/JNK pathway to modulate cellular metabolic responses, and activating inflammatory signaling and perturb contractile status of LMCs. Insulin resistant LECs produced less NO due to a decrease in eNOS phosphorylation and showed a significant decrease in impedance across an LEC monolayer that was associated with disruption in the adherence junctional proteins. Additionally, insulin resistance in LECs impaired mitochondrial function by decreasing basal-, maximal-, and ATP-linked-oxygen consumption rates and activated NF-κB nuclear translocation coupled with increased pro-inflammatory signaling. Additionally, insulin resistant LMCs exhibited elevated intracellular calcium and decreased striated muscle-specific sarcoplasmic reticulum Ca2+ ATPase 2a (SERCA2a)  expression and activity. SERCA2a expression was significantly decreased in MetSyn lymphatic vessels and a SERCA activator, CDN 1163 increased phasic contractile frequency in the vessels from MetSyn, thereby, partially restored lymph flow in MetSyn rats.
 

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Additional Information

In Campus Calendar
Yes
Groups

Parker H. Petit Institute for Bioengineering and Bioscience (IBB)

Invited Audience
Faculty/Staff, Postdoc, Public, Graduate students
Categories
Seminar/Lecture/Colloquium
Keywords
go-PetitInstitute, IBB
Status
  • Created By: Floyd Wood
  • Workflow Status: Published
  • Created On: Apr 2, 2019 - 10:42am
  • Last Updated: Apr 2, 2019 - 10:42am