G-Protein Coupled Receptors (GPCRs) and Cellular Waste Disposal System Promote Inflammation, Finds a New Study

G-Protein Coupled Receptors (GPCRs) and Cellular Waste Disposal System Promote Inflammation, Finds a New Study

G-protein coupled receptors are found in cell membrane which act as signal transducers and enable the cells to react with their external environment. Many drugs work in the body by impacting GPCR function which plays an important role in various physiological processes such as blood pressure, heart rate, smell, vision, taste, and even allergic responses. Dysfunction of GPCR may lead to several diseases which make it the largest target for approved drugs.

A recent study conducted at University of California San Diego School of Medicine has unveiled insights on how cells use their cellular waste removal system and GPCR to promote ubiquitin-mediated inflammatory signaling. New findings published in the journal Cell Reports states that some approved drugs for cancer can inhibit the cellular activities and be repurposed to treat vascular inflammation, which occurs due to the formation of artery-blocking plaques.

According to JoAnn Trejo, professor in the department of Pharmacology at UC Sand Diego School of medicine, GPCRs and inflammation were observed to be influenced by ubiquitination, a process essential for protein degradation and signaling.

Trejo and his colleagues studied endothelial cells to understand how GPCR function is affected by ubiquitination which instructs the cell’s waste disposal system to degrade the protein. However, new insights were discovered in GPRC function and role of ubiquitination.

The studied showed that GPRC activates into an E3 ligase, the enzyme responsible for ubiquitination and triggers a series of molecular events that activates another protein called p38 which promotes inflammation. However, activation of NEDD4-2 to promote ubiquitin-mediated inflammatory signaling is still not known.

Only a few drugs have received FDA approval for cancer treatment that are able to inhibit E3 ubiquitin ligases and some others are being tested in clinical trials, said Trejo. Further, he points out that considering the large amount of E3 ligases in the human body and their multiple functions, approval and clinical trials of E3-targeting drugs are relatively small.

According to the researchers, this is the first time to find out the role of E3 ligase in promoting vascular inflammation and it broadens the potential application of drugs that inhibit these enzymes.

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