Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

Yang, Dong; Lee, Kyung Suk; Ko, Chang Mann; Moh, Sang Hyun; Song, Jihyeok; Hur, Lucia C.; Cheon, Young Woo; Yang, Seung Ho; Choi, Yun Hee; Kim, Ki Woo

doi:10.1016/j.peptides.2015.12.010

Cited by 13 publications

(11 citation statements)

References 48 publications

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“…For instance, the thymic IL18R + Tregs (unlike their CD73 + IL18R – or CD73 – counterparts) upregulate the expression of several genes that are associated with control of tissue homeostasis. These genes include Tff1 reported to play a key role in the repair of gut epithelium ( Playford et al, 1996 ) , Pdgfb a potent mesenchymal cell mitogen that promotes tissue repair, and Penk (encoding proenkephalin A), which was shown to affect various biological processes including control of cell proliferation ( Cheng et al, 2010 ; Linner et al, 1995 ; Malendowicz et al, 2005 ; Zagon et al, 2011 ), tissue repair ( Bigliardi-Qi et al, 2006 ; Yang et al, 2016 ), or adipocyte metabolism/function ( Brestoff et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

IL18 signaling promotes homing of mature Tregs into the thymus

Peligero-Cruz

Givony

Sebé-Pedrós

et al. 2020

eLife

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Foxp3+ regulatory T cells (Tregs) are potent suppressor cells, essential for the maintenance of immune homeostasis. Most Tregs develop in the thymus and are then released into the immune periphery. However, some Tregs populate the thymus and constitute a major subset of yet poorly understood cells. Here we describe a subset of thymus recirculating IL18R+ Tregs with molecular characteristics highly reminiscent of tissue-resident effector Tregs. Moreover, we show that IL18R+ Tregs are endowed with higher capacity to populate the thymus than their IL18R– or IL18R–/– counterparts, highlighting the key role of IL18R in this process. Finally, we demonstrate that IL18 signaling is critical for the induction of the key thymus-homing chemokine receptor – CCR6 on Tregs. Collectively, this study provides a detailed characterization of the mature Treg subsets in the mouse thymus and identifies a key role of IL18 signaling in controlling the CCR6-CCL20-dependent migration of Tregs into the thymus.

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Section: Discussionmentioning

confidence: 99%

IL18 signaling promotes homing of mature Tregs into the thymus

Peligero-Cruz

Givony

Sebé-Pedrós

et al. 2020

eLife

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“…A recent study also demonstrated the effects of morphine on cell migration, viability, and proliferation in oral epithelial cells [ 14 ]. Moreover, we previously observed that leucine-enkephalin promotes wound healing through regulating hemidesmosome and the expression of MMPs [ 37 ]. An essential role of μ-, κ-, and δ-opioid receptor in skin homeostasis including differentiation, proliferation, and migration has been investigated using knockout animal [ 10 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

β-Neoendorphin Enhances Wound Healing by Promoting Cell Migration in Keratinocyte

Yang

Moh²,

Choi

et al. 2020

Molecules

Self Cite

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The skin is the largest and a remarkably plastic organ that serves as a protective barrier against environmental stimuli and injuries throughout life. Skin injuries are serious health problems, and wound healing is a critical process to replace devitalized cellular and tissue structures. Although some endogenous opioids are known to be involved in the modulation of wound healing, it remains to be determined whether the β-neoendorphin (β-NEP), an endogenous opioid, has beneficial effects on wound repair in human keratinocyte. In this study, we found that β-NEP accelerated wound repair through activation of mitogen-activated protein kinase (MAPK)/Erk1/2 signaling pathways in human keratinocytes. Moreover, the wound healing effect of β-NEP is mainly through the acceleration of keratinocyte migration without affecting cell proliferation. Therefore, our studies reveal that β-NEP plays an important role in the regulation of wound repair and suggest a therapeutic strategy to promote wound healing using β-NEP.

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“…Reaux-Le Goazigo et al (Reaux-Le Goazigo et al 2019 ) also showed in mouse models that topical administration of endogenous opioid peptide-degrading enzyme inhibitor seemed to significantly alleviate corneal pain and inflammation (Giannaccare et al 2021 ; Reaux-Le Goazigo et al 2019 ). Furthermore, it was found that Leu-enkephalin (derived from the same aforementioned endogenous opioid peptide precursors) could also facilitate wound repair through the modulation of matrix metalloproteases (Yang et al 2016 ), thereby decelerating the extracellular matrix degradation process (Giannaccare et al 2021 ). Extracellular matrix is an important medium, as this is where the locus of pain sensation by C-fibers correlates more strongly with the harsher tissue damage experienced in the secondary non-contact injury phase.…”

Section: Tertiary Injury Phase: Ganglionopathymentioning

confidence: 99%

Is the Sex Difference a Clue to the Pathomechanism of Dry Eye Disease? Watch out for the NGF-TrkA-Piezo2 Signaling Axis and the Piezo2 Channelopathy

2022

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Dry eye disease (DED) is a multifactorial disorder with recognized pathology, but not entirely known pathomechanism. It is suggested to represent a continuum with neuropathic corneal pain with the paradox that DED is a pain-free disease in most cases, although it is regarded as a pain condition. The current paper puts into perspective that one gateway from physiology to pathophysiology could be a Piezo2 channelopathy, opening the pathway to a potentially quad-phasic non-contact injury mechanism on a multifactorial basis and with a heterogeneous clinical picture. The primary non-contact injury phase could be the pain-free microinjury of the Piezo2 ion channel at the corneal somatosensory nerve terminal. The secondary non-contact injury phase involves harsher corneal tissue damage with C-fiber contribution due to the lost or inadequate intimate cross-talk between somatosensory Piezo2 and peripheral Piezo1. The third injury phase of this non-contact injury is the neuronal sensitization process with underlying repeated re-injury of the Piezo2, leading to the proposed chronic channelopathy. Notably, sensitization may evolve in certain cases in the absence of the second injury phase. Finally, the quadric injury phase is the lingering low-grade neuroinflammation associated with aging, called inflammaging. This quadric phase could clinically initiate or augment DED, explaining why increasing age is a risk factor. We highlight the potential role of the NGF-TrkA axis as a signaling mechanism that could further promote the microinjury of the corneal Piezo2 in a stress-derived hyperexcited state. The NGF-TrkA-Piezo2 axis might explain why female sex represents a risk factor for DED.

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Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

Cited by 13 publications

References 48 publications

IL18 signaling promotes homing of mature Tregs into the thymus

IL18 signaling promotes homing of mature Tregs into the thymus

β-Neoendorphin Enhances Wound Healing by Promoting Cell Migration in Keratinocyte

Is the Sex Difference a Clue to the Pathomechanism of Dry Eye Disease? Watch out for the NGF-TrkA-Piezo2 Signaling Axis and the Piezo2 Channelopathy

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