Role of transforming growth factor-β in peripheral nerve regeneration

Ding, Zihan; Jiang, Meng; Qian, Jiaxi; Gu, Donghwan; Bai, Hao; Cai, Min; Yao, Dengbing

doi:10.4103/1673-5374.377588

Cited by 6 publications

(4 citation statements)

References 147 publications

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“…Therefore, the increased expression of inflammatory genes within the mid-distal graft of long ANAs could limit axonal growth. On the other hand, the expression of Tgf-β has been suggested to promote SC proliferation, the secretion of neurotrophic factors, and the modulation of immune cells into an anti-inflammatory phenotype [ 47 , 48 , 49 , 50 ]. The addition of exogenous Tgf-β after nerve injury also promotes SC reactivation and axonal regeneration in vivo [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Limited Nerve Regeneration across Acellular Nerve Allografts (ANAs) Coincides with Changes in Blood Vessel Morphology and the Development of a Pro-Inflammatory Microenvironment

Acevedo Cintrón,

Hunter,

Schellhardt

et al. 2024

IJMS

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The use of acellular nerve allografts (ANAs) to reconstruct long nerve gaps (>3 cm) is associated with limited axon regeneration. To understand why ANA length might limit regeneration, we focused on identifying differences in the regenerative and vascular microenvironment that develop within ANAs based on their length. A rat sciatic nerve gap model was repaired with either short (2 cm) or long (4 cm) ANAs, and histomorphometry was used to measure myelinated axon regeneration and blood vessel morphology at various timepoints (2-, 4- and 8-weeks). Both groups demonstrated robust axonal regeneration within the proximal graft region, which continued across the mid-distal graft of short ANAs as time progressed. By 8 weeks, long ANAs had limited regeneration across the ANA and into the distal nerve (98 vs. 7583 axons in short ANAs). Interestingly, blood vessels within the mid-distal graft of long ANAs underwent morphological changes characteristic of an inflammatory pathology by 8 weeks post surgery. Gene expression analysis revealed an increased expression of pro-inflammatory cytokines within the mid-distal graft region of long vs. short ANAs, which coincided with pathological changes in blood vessels. Our data show evidence of limited axonal regeneration and the development of a pro-inflammatory environment within long ANAs.

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Section: Discussionmentioning

confidence: 99%

Limited Nerve Regeneration across Acellular Nerve Allografts (ANAs) Coincides with Changes in Blood Vessel Morphology and the Development of a Pro-Inflammatory Microenvironment

Acevedo Cintrón,

Hunter,

Schellhardt

et al. 2024

IJMS

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“…TGF is a protein composed of amino acids in the cytoplasm, belonging to the family of peptide growth factors. It includes two main types: TGF-α and TGF-β ( 92 ). TGF-α has been described in the EGF section.…”

Section: Growth Factors Involved In Repair Mechanismsmentioning

confidence: 99%

Elucidating the mechanism of corneal epithelial cell repair: unraveling the impact of growth factors

Gong,

Ding,

Hao

et al. 2024

Front. Med.

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The repair mechanism for corneal epithelial cell injuries encompasses migration, proliferation, and differentiation of corneal epithelial cells, and extracellular matrix remodeling of the stromal structural integrity. Furthermore, it involves the consequential impact of corneal limbal stem cells (LSCs). In recent years, as our comprehension of the mediating mechanisms underlying corneal epithelial injury repair has advanced, it has become increasingly apparent that growth factors play a pivotal role in this intricate process. These growth factors actively contribute to the restoration of corneal epithelial injuries by orchestrating responses and facilitating specific interactions at targeted sites. This article systematically summarizes the role of growth factors in corneal epithelial cell injury repair by searching relevant literature in recent years, and explores the limitations of current literature search, providing a certain scientific basis for subsequent basic research and clinical applications.

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“…WD is a relatively rapid and complex process in the PNS, triggering structural changes in distal myelin sheaths and axons within a few hours of injury, followed by gradual disintegration, increased phagocytosis, and the removal of damaged myelin and axons from the lesion over the next few days [ 18 ]. WD is also a process in which multiple active substances and cells are involved and axonal disintegration actively occurs [ 19 , 20 ]. During the phase of WD, SCs in vivo are activated to dedifferentiate, while immune-related cells such as neutrophils and macrophages are recruited to the lesion site [ 21 ].…”

Section: Inflammatory Response After Nerve Injurymentioning

confidence: 99%

Inflammation in the Peripheral Nervous System after Injury

Gu,

Xia,

Ding

et al. 2024

Biomedicines

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Nerve injury is a common condition that occurs as a result of trauma, iatrogenic injury, or long-lasting stimulation. Unlike the central nervous system (CNS), the peripheral nervous system (PNS) has a strong capacity for self-repair and regeneration. Peripheral nerve injury results in the degeneration of distal axons and myelin sheaths. Macrophages and Schwann cells (SCs) can phagocytose damaged cells. Wallerian degeneration (WD) makes the whole axon structure degenerate, creating a favorable regenerative environment for new axons. After nerve injury, macrophages, neutrophils and other cells are mobilized and recruited to the injury site to phagocytose necrotic cells and myelin debris. Pro-inflammatory and anti-inflammatory factors involved in the inflammatory response provide a favorable microenvironment for peripheral nerve regeneration and regulate the effects of inflammation on the body through relevant signaling pathways. Previously, inflammation was thought to be detrimental to the body, but further research has shown that appropriate inflammation promotes nerve regeneration, axon regeneration, and myelin formation. On the contrary, excessive inflammation can cause nerve tissue damage and pathological changes, and even lead to neurological diseases. Therefore, after nerve injury, various cells in the body interact with cytokines and chemokines to promote peripheral nerve repair and regeneration by inhibiting the negative effects of inflammation and harnessing the positive effects of inflammation in specific ways and at specific times. Understanding the interaction between neuroinflammation and nerve regeneration provides several therapeutic ideas to improve the inflammatory microenvironment and promote nerve regeneration.

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Role of transforming growth factor-β in peripheral nerve regeneration

Cited by 6 publications

References 147 publications

Limited Nerve Regeneration across Acellular Nerve Allografts (ANAs) Coincides with Changes in Blood Vessel Morphology and the Development of a Pro-Inflammatory Microenvironment

Limited Nerve Regeneration across Acellular Nerve Allografts (ANAs) Coincides with Changes in Blood Vessel Morphology and the Development of a Pro-Inflammatory Microenvironment

Elucidating the mechanism of corneal epithelial cell repair: unraveling the impact of growth factors

Inflammation in the Peripheral Nervous System after Injury

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