Arthritis-related gene also regenerates cartilage in joints and growth plates (IL-6 & STAT3, which antioxidants reduce and NAC can increase)

Medical Xpress / University of Southern California / Communications Biology ^ | Jan. 17, 2022 | Cristy Lytal, Nancy Q. Liu et al

[ConservativeMind]

IL-6 family proteins can promote inflammation, arthritis, autoimmune disease and even cancer. However, a study reveals the importance of IL-6 and associated genes for maintaining and regenerating cartilage in both the joints and in the growth plates that enable skeletal growth in children.

"We show that the IL-6 family, previously associated with arthritis, bone and muscle loss, and other chronic inflammatory diseases, is required for the maintenance of skeletal stem and progenitor cells, and for the healthy growth and function of the joints and spine," said author Denis Evseenko. "Our study establishes a link between inflammation and regeneration, and may explain why stem and progenitors are exhausted in chronic inflammation."

In the study, colleagues took a close look at a key gene activated by IL-6: STAT3. In both lab-grown human cells and in mice, the scientists demonstrated that STAT3 is critical for the proliferation, survival, maturation and regeneration of cartilage-forming cells in the joints and growth plates. When the gene ceased to function, cartilage-forming cells became increasingly dysfunctional over time, resulting in smaller body size, prematurely fused growth plates, underdeveloped skeletons and mildly degenerated joint cartilage.

Mice experienced the same issues when they lacked a protein called glycoprotein 130 (gp130), which all IL-6 proteins use to activate Stat3. Deactivating another gene Lifr, which encodes a protein that works with gp130 to recognize one of the IL-6 proteins called Lif, produced similar but milder skeletal and cartilage changes.

In mice lacking gp130, the scientists could restore normal growth plates by over-activating Stat3—although this also caused an overgrowth of cartilage that led to other skeletal abnormalities.

The study has clinical implications for the use of existing drugs that inhibit STAT3 to curb inflammation in autoimmune diseases: these drugs may also interfere with growth and regeneration.

[ConservativeMind]

This is an interesting issue, as it would appear having to constant a stream of antioxidants could affect how quickly we lose our cartilage, over time.

Interestingly, NAC can counter other antioxidants and increases STAT3 and IL-6, as I’ll next post a study on that.

[ConservativeMind]

N-Acetyl cysteine prevents activities of STAT3 inhibitors, Stattic and BP-1-102 independently of its antioxidant properties

https://pubmed.ncbi.nlm.nih.gov/31627175/

[ConservativeMind]

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[married21]

And here I thought the NAC was a rock band.

[Magic Fingers]

This is an interesting issue, as it would appear having to constant a stream of antioxidants could affect how quickly we lose our cartilage, over time.

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Seems like a “between a rock and a hard place” scenario.

[glorgau]

In mice lacking gp130, the scientists could restore normal growth plates by over-activating Stat3—although this also caused an overgrowth of cartilage that led to other skeletal abnormalities.

Sounds like a grand opportunity to try site specific delivery using nano particles.

[RushIsMyTeddyBear]

Bkmrk

[Irish Eyes]

Bookmark

[KSCITYBOY]

btt

[Boogieman]

Ok, this is some gene therapy I might take if it can fix my bum knee and lower back :)

[sauropod]

bkmk

[saintgermaine]

You sound just like me. It is my back, left hip and left knee.

[theirjustdue]

Please add me to your list. Thank you.