The role of keratinocyte function on the defected diabetic wound healing

Mansoub, Navid Hosseini

doi:10.5603/dk.a2022.0004

Cited by 11 publications

(5 citation statements)

References 65 publications

(106 reference statements)

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“…Additionally, SDF-1α seems to directly influence keratinocyte capacity for proliferation positively 20 . This supports wound healing and more precisely expressed reepithelialization, as high blood glucose level in diabetes impairs proliferative rate of keratinocytes at least in vitro 21 , 22 .…”

Section: Introductionsupporting

confidence: 65%

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

Sommer

Jakob

Lettenmeier

et al. 2023

Sci Rep

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Chronic non healing wounds in diabetic patients still impose a major problem in modern medicine. Especially additional peripheral vascular disease complicates treatment success in these patients. Thus, we analyzed the effects of 11,12 epoxyeicosatrienoic acid (EET) in a combined model of hyperglycemia and ischemia in mice. Hyperglycemia was induced by Streptozotozin 2 weeks prior to wounding. 3 days before wound creation 2 of the 3 suppling vessels of the moue ear were cautherized for ischemia. Either 11,12 EET or solvent for control was applied. Wound closure as well as TNF-α, TGF-β, SDF-1α, VEGF, CD31, and Ki67 were measured. The wounds closed on day 14.4 ± 0.4 standard deviation (SD). 11,12 EET treatment enhanced healing to 9.8 ± 0.6 SD. TNF-α level was augmented on day 9 compared to control and receded on day 18. TGF-β seemed to be elevated all days observed after 11,12 EET treatment. SDF-1α was enhanced on day 6 and 9 by 11,12 EET, and VEGF on day 6 and 18 as well as CD13 on day 3, 6, and 18. 11,12 EET did not alter Ki67. 11,12 EET are able to rescue deteriorated wound healing in a combined model of hyperglycamia and ischemia by resolution of inflammation, augmentation of neovascularization and increasing expression of TGF-β as well as SDF-1α.

show abstract

Section: Introductionsupporting

confidence: 65%

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

Sommer

Jakob

Lettenmeier

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Additionally, SDF-1α seems to directly in uence keratinocyte capacity for proliferation positively 20 . This support wound healing and more precisely expressed reepithelialization, as high blood glucose level in diabetes impairs proliferative rate of keratinocytes at least in vitro 21,22 .…”

Section: Introductionmentioning

confidence: 77%

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

Sommer

Jakob

Lettenmeier

et al. 2023

Preprint

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Chronic non-healing wounds caused by diabetes and ischemia. We analyzed the effects of 11,12 Epoxyeicosatrienoic acid (EET) in a combined model of hyperglycemia and ischemia in mice. Hyperglycemia was induced by Streptozotozin 2 weeks prior to wounding. 3 days before wound creation 2 of the 3 suppling vessels of the moue ear were cautherized for ischemia. Either 11,12 EET or solvent for control was applied. Wound closure as well as TNF-α, TGF-β, SDF-1α, VEGF, CD31, and Ki67 was measured. The wounds closed on day 14.4 ± 0.4 standard deviation (SD). 11,12 EET treatment enhanced healing to 9.8 ± 0.6 SD. TNF-α level was augmented on day 9 compared to control and receded on day 18. TGF-β seemed to be elevated all days observed after 11,12 EET treatment. SDF-1α was enhanced on day 6 and 9 by 11,12 EET, and VEGF on day 6 and 18 as well as CD13 on day 3, 6, and 18. 11,12 EET did not alter Ki67. 11,12 EET are able to rescue deteriorated wound healing in a combined model of hyperglycamia and ischemia by resolution of inflammation, augmentation of neovascularization and increasing expression of TGF-β as well as SDF-1α.

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“…Keratinocytes are the main cell type in the epidermis layer of the skin. They not only act as an effective barrier but also actively participate in mediating skin inflammatory reactions and interacting with immune cells 30 and play a key role in regulating chronic wound inflammation 31 , 32 . At present, the most common clinical methods to suppress the inflammatory reaction of DFU include incision decompression, drainage of the abscess, antibiotic treatment, and nanomaterial-based treatment strategies 12 , 33 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-221-3p inhibits the inflammatory response of keratinocytes by regulating the DYRK1A/STAT3 signaling pathway to promote wound healing in diabetes

Hu,

Liu,

Tang

et al. 2024

Commun Biol

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Diabetic foot ulcer (DFU), a serious complication of diabetes, remains a clinical challenge. MicroRNAs affect inflammation and may have therapeutic value in DFU. Here, we find that an miR-221-3p mimic reduces the inflammatory response and increases skin wound healing rates in a mouse model of diabetes, whereas miR-221-3p knockout produced the opposite result. In human keratinocytes cells, miR-221-3p suppresses the inflammatory response induced by high glucose. The gene encoding DYRK1A is a target of miR-221-3p. High glucose increases the expression of DYRK1A, but silencing DYRK1A expression decreases high glucose–induced inflammatory cytokine release via dephosphorylation of STAT3, a substrate of DYRK1A. Application of miR-221-3p mimic to human keratinocytes cells not only decreases DYRK1A expression but also inhibits high glucose–induced production of inflammatory cytokines to promote wound healing. This molecular mechanism whereby miR-221-3p regulates inflammation through the DYRK1A/STAT3 signaling pathway suggests targets and therapeutic approaches for treating DFU.

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The role of keratinocyte function on the defected diabetic wound healing

Abstract: This article has been peer reviewed and published immediately upon acceptance.It is an open access article, which means that it can be downloaded, printed, and distributed freely, provided the work is properly cited.

Cited by 11 publications

References 65 publications

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

Various effects of 11,12 EET rescue wound healing in a combined model of diabetes and ischemia

MicroRNA-221-3p inhibits the inflammatory response of keratinocytes by regulating the DYRK1A/STAT3 signaling pathway to promote wound healing in diabetes

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