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USA: A recent study published in Science Signaling has revealed that a pannexin channel protein may be protective against obesity-related hypertension.

Endothelial pannexin 3 (Panx3) and Bcl6 abundance were reduced in hypertensive, obese individuals, indicating that reductions in endothelial Panx3 may drive obesity-associated hypertension.

"Our findings provide insight into a channel-independent role of Panx3 wherein its interaction with Bcl6 determines vascular oxidative state, particularly under the adverse conditions of obesity," Abigail G. Wolpe, University of Virginia School of Medicine, Charlottesville, VA, USA, and colleagues wrote.

Obesity induces endothelial dysfunction that can result in hypertension. Dr. Wolpe and the team uncovered a role for Panx3 as a scaffolding protein that limits oxidative stress in the endothelium and hypertension.

Panx3 bound to and stabilized the transcriptional repressor Bcl6, which suppressed Nox4 expression, the gene encoding a hydrogen peroxide–producing enzyme. Mice lacking Panx3 in endothelial cells or treated with a peptide that disrupted the Panx3-Bcl6 interaction demonstrated greater oxidative stress in the endothelium and developed hypertension. Furthermore, there was a decrease in Panx3 mRNA expression and Bcl6 protein abundance, and Nox4 mRNA expression was increased in mice with diet-induced obesity, but not in mice with pharmacologically induced hypertension.

In the study, the researchers report that the abundance of endothelial Bcl6 is determined by its interaction with Golgi-localized Panx3 and that Bcl6 transcriptional activity protects against vascular oxidative stress.

Key observations were as follows:

• Consistent with data from obese, hypertensive humans, mice with an endothelial cell–specific deficiency in Panx3 had spontaneous systemic hypertension without obvious changes in channel function, as assessed by Ca2+ handling, ATP amounts, or Golgi luminal pH.
• Panx3 bound to Bcl6, and its absence reduced Bcl6 protein abundance, suggesting that the interaction with Panx3 stabilized Bcl6 by preventing its degradation.
• Panx3 deficiency was associated with increased gene expression encoding the H2O2-producing enzyme Nox4, normally repressed by Bcl6, resulting in H2O2-induced oxidative damage in the vasculature.
• Catalase rescued impaired vasodilation in mice lacking endothelial Panx3. Administration of a newly developed peptide to inhibit the Panx3-Bcl6 interaction recapitulated the increase in Nox4 expression and blood pressure in mice with endothelial Panx3 deficiency.
• Panx3-Bcl6-Nox4 dysregulation occurred in obesity-related hypertension, but not when hypertension was induced in the absence of obesity.

Using pharmacological and genetic approaches, the researchers demonstrated the Panx3-Bcl6 interaction as a regulator of vascular oxidative stress and systemic blood pressure. The study findings illuminate the dysregulation of Panx3/Bcl6/Nox4 as a pathway by which obesity can drive endothelial dysfunction and hypertension.

"Together, these data suggest that Panx3 oligomers exhibit diverse stoichiometric," the research group concluded. "In the endothelium, there is no direct evidence for channel functionality, and we instead posit that Golgi-localized Panx3 protects against oxidative stress in the cardiovascular system through protein-protein interactions with Bcl6."

Reference:

Wolpe, A. G., Luse, M. A., Baryiames, C., Schug, W. J., Wolpe, J. B., Johnstone, S. R., Dunaway, L. S., Juśkiewicz, Z. J., Loeb, S. A., Askew Page, H. R., Chen, L., Sabapathy, V., Pavelec, C. M., Wakefield, B., Cifuentes-Pagano, E., Artamonov, M. V., Somlyo, A. V., Straub, A. C., Sharma, R., . . . Isakson, B. E. (2024). Pannexin-3 stabilizes the transcription factor Bcl6 in a channel-independent manner to protect against vascular oxidative stress. Science Signaling. https://doi.org/adg2622

ts implanted with the Micropure IOL (BVI). Average induced astigmatism was 1 D at 3 months, and 80% of patients were within 1 D of intended correction, with similar outcomes and a tendency for

Michael, who is AbbVie's chief operating officer, will become the company's second-ever CEO since the company spun out from Abbott Laboratories in 2013. 

The doctor's lifeless body was found after the locals spotted it floating in a drain and immediately alerted the police. Upon receiving the report, the police rushed to the spot along with forensic experts of the Field Unit.

Also read- NMCH Senior Doctor Goes Missing, Family Lodges Kidnapping Case In Patna

As per a TOI news report, the police were searching for the doctor for a week, leading to the start of a search operation in order to find her but failed. After the recovery of her body, the police reached out to the doctor's relatives and obtained confirmation of her identity.

According to the father's statement, the doctor was suffering from depression and had a tendency to end her life. It emerged that she had earlier attempted suicide several times but failed. 

However, this time, the doctor went outside from her house informing her parents that she was going for a walk and went missing. It is unclear whether she committed suicide or if any foul play was involved. The results of her postmortem examination will help the police in determining the cause for her passing.

"My daughter was a little introvert and she had attempted suicide several times before. She was suffering from depression for a long and was undergoing treatment in Fatehgarh. Eight years ago, while on her way for medical treatment, she had tried to commit suicide by jumping off a train near Shamsabad,” her father informed the daily.

“On Feb 9, she jumped into a drain near her room in Azamgarh. We then brought her to Kanpur on Feb 10. On Feb 11 morning, Richa left the house saying that she was going for a walk and did not return. After inquiring with neighbours and relatives, the family lodged a missing complaint at Gujaini police station,” he added.

A case was registered at the Gujaini police station under section 154 Criminal Procedure Code, 1973 but the police failed to trace her. 

Talking about the case, Gujaini police station in-charge Vinay Tiwari said “Further investigations are underway to ascertain the exact cause of the woman’s death."

Also read- NMCH Doctor Missing Case: Bollywood Actor Shekhar Suman Demands CBI Probe

The whole genome sequencing data from a wide range of Americans aims to address the historical lack of diversity in existing genomic datasets by focusing on previously under-represented groups. The U.S. National Institutes of Health-funded "All of Us" study turned up 1 billion genetic variants in total.

"Sequencing diverse populations can lead to new drug targets that are relevant to everyone," said Dr. Josh Denny, a study author and its chief executive. "It can also help uncover disparities that lead to specific treatments for people that are experiencing higher burdens of disease or different disease."

NEW STUDY FINDS DYSLEXIA IS LINKED TO 42 GENETIC VARIANTS

Although many genetic variants have no impact on health, nearly 4 million of the newly discovered differences in the genetic code are located in areas that may be tied to disease risk, the researchers reported in a series of papers published in Nature and related journals.

"This is huge," said Denny. The study aims to eventually collect DNA and other health data on 1 million people in hopes of better understanding genetic influences on health and disease.

Nearly 90% of genomic studies to date have been done in people of European ancestry, which has led to a narrow understanding of the biology of diseases and slowed the development of drugs and prevention strategies effective in diverse populations, the leaders of several NIH departments wrote in a related commentary.

"It's a huge gap, obviously, because most of the world's population is not of European ancestry," Denny said.

Recent studies have already shown how genetic diversity can impact disease risk. Variants in the APOL1 gene discovered in 2010 help account for 70% of the increased risk for chronic kidney disease and dialysis seen in people in the U.S. with sub-Saharan African ancestry.

Likewise, a class of drugs called PCSK9 inhibitors that dramatically lower very high levels of low-density lipoprotein (LDL) - the so-called bad cholesterol - were discovered by sequencing the genetic code of 5,000 people in Dallas of African ancestry.

Much more work is needed to understand how the new trove of genetic variants contributes to various health conditions, but the scientists believe they could be used to refine tools used to calculate a person's risk for disease.

On Monday, February 19, the team from the Vector Control Unit will visit a number of districts in St Andrew. They are Corbin’s Road, Lakes Road, Farrell Road, Isolation Road, Jordan Road, Franklin Doughlin Road, Babylon Road, Walkers, Bawden’s Road, and environs.

The following areas in St Peter will be fogged on Tuesday, February 20: French Village, Mount Brevitor, West Ring Road, Vuemont, Bow Drive, Inner Circle, Mile- and- a- Quarter, and surrounding districts.

On Wednesday, February 21, the St Peter districts of Maynard’s Road, Maynard’s Housing Area, Leslie Gardens, Carpenter’s Circle, Rose Hill, and environs will be sprayed.

The team will target the St Lucy districts of Trent’s Road, Hannays Road, Swampy Town, Hope Bridge Road, and neighbouring areas on Thursday, February 22.

Fogging will conclude for the week on Friday, February 23, in St Thomas in White Hall Road, Country View, Hill View Drive, and environs.

Fogging takes place from 4:30 to 8:30 p.m. daily. Householders are reminded to open their windows and doors to allow the spray to enter. Children should not be allowed to play in the spray.

Members of the public are advised that the completion of scheduled fogging activities may be affected by events beyond the Unit’s control. In such circumstances, it will return to communities affected in the soonest possible time.

(PR)

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