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Beta Thymosins: The Role in Immunity, Organ Regeneration, Development and...
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Beta Thymosins: The Role in Immunity, Organ Regeneration, Development and Aging

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 March 2024) | Viewed by 4431

Special Issue Editor

Dr. Ildiko Bock-Marquette

E-Mail Website
Guest Editor
Department of Biochemistry and Medical Chemistry, Szentagothai Research Centre, University of Pecs, Pecs, Hungary
Interests: beta thymosins; development; organ regeneration; clinical translation; stress; aging

Special Issue Information

Dear Colleagues,

To instantiate novel direction and effectively reverse cellular damage in adult mammals has been a dream among scientists for a long time. Many believe that utilization of naturally existing small, secreted molecules may potentially present the solution. Here, we kindly invite you to contribute and participate in an upcoming Special Issue of IJMS focusing on a group of molecules, referred to as beta thymosins, a family of highly conserved acidic 5kDa peptides, originally thought to be thymic hormones, notably, first described in 1966 by A.L. Goldstein and A. White. Since their discovery, this group of exciting molecules has become a target of a vast number of outstanding international investigations. According to the present literature, beta thymosins are widely expressed among various tissues and cell types of the body. The first investigations were communicated by Lin and colleagues in 1990. Since then, numerous results have been published suggesting the ubiety of beta thymosins among various species, including fish, chickens, or even humans. The impressive collection of amassed data regarding the peptides’ role during embryonic development doubtlessly imply a significant impact during adult organ regeneration and repair.

This Special Issue seeks manuscript submissions furthering our understanding or summarizing the current knowledge describing the role of beta thymosins regarding clinical translation, their impact on health and regeneration, immunity, development, and aging.

Dr. Ildiko Bock-Marquette
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • beta thymosins
  • organ regeneration
  • immunity and inflammation
  • development
  • aging

Published Papers (2 papers)

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Research

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16 pages, 4283 KiB  
Article
Thymosin Beta 4 Inhibits LPS and ATP-Induced Hepatic Stellate Cells via the Regulation of Multiple Signaling Pathways
by Jihye Choi, Yunsang Cho, Hwal Choi, Sangmin Lee, Hyeju Han, Jeonghyeon Lee and Jungkee Kwon
Int. J. Mol. Sci. 2023, 24(4), 3439; https://doi.org/10.3390/ijms24043439 - 08 Feb 2023
Cited by 6 | Viewed by 2028
Abstract
Risk signals are characteristic of many common inflammatory diseases and can function to activate nucleotide-binding oligomerization (NLR) family pyrin domain-containing 3 (NLRP3), the innate immune signal receptor in cytoplasm. The NLRP3 inflammasome plays an important role in the development of liver fibrosis. Activated [...] Read more.
Risk signals are characteristic of many common inflammatory diseases and can function to activate nucleotide-binding oligomerization (NLR) family pyrin domain-containing 3 (NLRP3), the innate immune signal receptor in cytoplasm. The NLRP3 inflammasome plays an important role in the development of liver fibrosis. Activated NLRP3 nucleates the assembly of inflammasomes, leading to the secretion of interleukin (IL)-1β and IL-18, the activation of caspase-1, and the initiation of the inflammatory process. Therefore, it is essential to inhibit the activation of the NLRP3 inflammasome, which plays a vital role in the immune response and in initiating inflammation. RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5′-triphosphate (ATP) to activate the NLRP3 inflammasome. Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added. As a result, we investigated the effects of Tβ4 on the NLRP3 inflammasome. Tβ4 prevented LPS-induced NLRP3 priming by inhibiting NF-kB and JNK/p38 MAPK expression and the LPS and ATP-induced production of reactive oxygen species. Moreover, Tβ4 induced autophagy by controlling autophagy markers (LC3A/B and p62) through the inhibition of the PI3K/AKT/mTOR pathway. LPS combined with ATP significantly increased thee protein expression of inflammatory mediators and NLRP3 inflammasome markers. These events were remarkably suppressed by Tβ4. In conclusion, Tβ4 attenuated NLRP3 inflammasomes by inhibiting NLRP3 inflammasome-related proteins (NLRP3, ASC, IL-1β, and caspase-1). Our results indicate that Tβ4 attenuated the NLRP3 inflammasome through multiple signaling pathway regulations in macrophage and hepatic stellate cells. Therefore, based on the above findings, it is hypothesized that Tβ4 could be a potential inflammatory therapeutic agent targeting the NLRP3 inflammasome in hepatic fibrosis regulation. Full article
(This article belongs to the Special Issue Beta Thymosins: The Role in Immunity, Organ Regeneration, Development and Aging)
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Review

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13 pages, 2282 KiB  
Review
The Pathophysiological Role of Thymosin β4 in the Kidney Glomerulus
by William J. Mason and Elisavet Vasilopoulou
Int. J. Mol. Sci. 2023, 24(9), 7684; https://doi.org/10.3390/ijms24097684 - 22 Apr 2023
Cited by 1 | Viewed by 1789
Abstract
Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease progression. New strategies are needed [...] Read more.
Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease progression. New strategies are needed to slow the progression to end-stage kidney disease, which requires dialysis or transplantation. Thymosin β4 (Tβ4), an endogenous peptide that sequesters G-actin, has shown potent anti-inflammatory function in experimental models of heart, kidney, liver, lung, and eye injury. In this review, we discuss the role of endogenous and exogenous Tβ4 in glomerular disease progression and the current understanding of the underlying mechanisms. Full article
(This article belongs to the Special Issue Beta Thymosins: The Role in Immunity, Organ Regeneration, Development and Aging)
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