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The mechanism by which inflammation causes disruption of circadian rhythms

 Last Update: 2022-08-10
 Source: Internet
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Summary

The circadian clock regulates tissue homeostasis through the temporal control of tissue-specific clock-controlling gen.

In articular cartilage, circadian rhythm disturbances are associated with a pro-metabolic sta.

Introduction

The circadian clock is an intrinsic genetic timing mechanism that is present in the brain and nearly all peripheral tissue cells and operates within approximately 24 hou.

The circadian clock coordinates the physiological activity of specific tissues through different cycles such as light and dark, body temperature, rest and activity (1

The circadian clock drives the expression of many other genes, known as clock-controlling genes, which are tissue-specific and play an important role in maintaining tissue homeostasis through their temporal properti.

4,9

Induces extracellular matrix degradation by promoting the production of degradative enzymes and other pro-inflammatory mediators, thereby shifting chondrocyte activity to a pro-metabolic state (25–29

38–40), we address these limitations using genetic engineering to develop various self-regulating cellular systems (41

20) cartilage degeneration (18) Due to disturbances in circadian rhythms, and the recent discovery that inflammation can drive disruption of circadian rhythms in chondrocytes, the goal of this study was to develop tissue engineered cartilage using genetically engineered stem cells to maintain the circadian rhythm of the inflammatory respon.

Inflammation disrupts circadian clock in native and tissue engineered cartilage

Next, we investigated the effect of inflammatory cytokines IL-1α, IL-1β and TNFα on the circadian rhythm of tissue engineered cartilage granul.

Anti-IL-1 genetically engineered tissue protects against circadian rhythm disturbances

Cartilage explants treated with IL-1α and IL-1β restored the loss of circadian rhythm by adding the anti-inflammatory agent dex (F.

discuss

By combining tissue engineering, synthetic biology, and circadian biology, we have developed cell-based tissue structures that preserve the cartilage circadian clock in response to damaging stimuli such as IL-1-induced inflammati.

While significant progress has been made in understanding the physiology of the circadian clock in recent years, genetic approaches have not previously been used to create cell-based clock-preserving therapeutic syste.

This is consistent with previous reports that mouse embryonic stem cells and other stem/progenitor cells fail to develop circadian rhythms prior to differentiation (46) suggest that the formation of a mature circadian clock is an integral feature of cell differentiati.

Here, we show the different responses of chondrocytes to circadian rhyth.

Many diseases are related to the disturbance of the biological clock (2,4,7,8
Using gene therapy approaches to create cell therapies that focus on preserving or synchronizing the circadian clock could be a useful weapon to help improve diseases beyond .

For example, in the presence of inflammation, these circuits can be used to protect other musculoskeletal tissues through IL-1-induced inflammation, such as the intervertebral disc, which displays a similar circadian rhythm and cytokine sensitivity to articular cartilage (2,54
Using tissue engineering and creating cells capable of maintaining circadian rhythms beyond inflammation-driven circuits opens up the possibility of developing additional engineered cell therapies for other diseases such as age-related circadian rhythm weakening or cancer (55,56) by maintaining the circadian clock and related genes involved in tissue homeostasis (4,9

Using an engineered tissue that protects itself from inflammation and maintains the circadian clock during the inflammatory response could overcome the limitations of current OA treatment and articular cartilage repa.

This work can be extended to create clock-preserving cell therapies across many tissues by differentiating developed iPSC strains into other tissues or using lentiviral approach.

For example, the NFκBr-IL1Ra lentiviral system has been used in miPSCs and primary porcine chondrocytes for inflammatory activation and mechanoreactive drug delivery (44,45
Future work in comparing rhythm transcripts and understanding the beneficial effects of rhythm preservation will provide further insights into the physiology of the cartilage clo.

This approach opens up an innovative frontier for creating cell-based therapeutics to maintain the biological clo.

In conclusion, this framework of developmental clock-preserving cellular systems provides a new self-regulatory approach to establish treatments and enhance tissue repa.

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