A new study from Karolinska Institutet and the Chinese Academy of Medical Sciences has identified an RNA molecule that is important for skin wound healing. The research, published in Nature Communications, may have implications for the treatment of hard-to-heal wounds.

The study focuses on the molecular processes in wound healing that regulate the transition from inflammation – a critical defence mechanism – to a proliferative phase, where new cells form to repair damaged tissue. Researchers have now mapped lncRNA (long non-coding RNA molecules) in human skin wounds in tissue samples from Karolinska University Hospital, identifying a key regulator in wound healing.

Guiding skin cells

“Our study reveals that the lncRNA molecule SNHG26 plays a pivotal role in guiding skin cells through the stages of wound healing, from an inflammatory stage to a healing phase,” explains Ning Xu Landén, docent at the Department of Medicine, Solna, Karolinska Institutet.

The researchers also used mouse models to uncover how this molecule interacts with genes involved in inflammation and tissue regeneration. In mice lacking SNHG26, wound healing was delayed, emphasising the molecule’s importance in the balance between inflammation and tissue repair. The discovery paves the way for new therapeutic approaches for acute and chronic wounds.

Single-cell transcriptomic analysis of impaired wound repair in Snhg26-KO mice

Fig. 3

a UMAP plot and cluster annotation of 21491 cells from skin and wounds of Snhg26-KO and WT mice (n = 3/group). b UMAP plot showing the expression of Snhg26 in Snhg26-KO and WT mice. c Violin plot showing the expression of Snhg26 in different cell types in WT mice. d Comparison of skin and wound cell composition between the KO and WT mice. Red line indicates keratinocyte clusters with changed cell composition in the wound of KO mice. Blue line indicates immune cell clusters. e The proportion of DEGs [log2(FC) ≥ 0.3, -log10(FDR) > 2] within all expressed genes in individual cell clusters in wounds of Snhg26-KO and WT mice. f GO and KEGG analysis of the top 200 marker genes in basal keratinocyte cell clusters. g The proliferation, migration, and inflammatory scores were plotted for each keratinocyte cluster. h–j Violin plots showing keratinocyte migration (h), proliferation (i) and inflammation scores (j) in Snhg26-KO and WT mice wound basal keratinocytes. k Circle plots displaying the CCL signaling network in Snhg26-KO and WT mice wounds. The changed signals in the KO mice compared to the WT mice were highlighted with arrows. The data were analyzed by two- sided post hoc test (c), two- sided Fisher’s exact test (f) or two-sided Mann-Whitney U test (h–j).

“By targeting SNHG26, we may be able to accelerate healing and reduce complications, particularly in chronic wounds where prolonged inflammation is a major problem,” says Ning Xu Landén.

Also studies microRNA

Her research group at Karolinska Institutet is studying how healing processes in the skin are controlled by so-called regulatory RNA molecules, i.e. RNA molecules that regulate gene activity and include both lncRNAs and the now Nobel Prize-awarded microRNA molecules. The researchers will now continue to study how other regulatory RNA molecules are involved in tissue repair, with the aim of developing innovative treatments for hard-to-heal wounds

Source – Karolinska Institutet

Li D, Liu Z, Zhang L, Bian X, Wu J, Li L, Chen Y, Luo L, Pan L, Kong L, Xiao Y, Wang J, Zhang X, Wang W, Toma M, Piipponen M, Sommar P, Xu Landén N. (2024) The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healing. Nat Commun 15(1):8637. [article]

Related Posts

A new study from Karolinska Institutet and the Chinese Academy of Medical Sciences has identified an RNA molecule that is important for skin wound healing. The research, published in Nature Communications, may have implications for the treatment of hard-to-heal wounds.

The study focuses on the molecular processes in wound healing that regulate the transition from inflammation – a critical defence mechanism – to a proliferative phase, where new cells form to repair damaged tissue. Researchers have now mapped lncRNA (long non-coding RNA molecules) in human skin wounds in tissue samples from Karolinska University Hospital, identifying a key regulator in wound healing.

Guiding skin cells

“Our study reveals that the lncRNA molecule SNHG26 plays a pivotal role in guiding skin cells through the stages of wound healing, from an inflammatory stage to a healing phase,” explains Ning Xu Landén, docent at the Department of Medicine, Solna, Karolinska Institutet.

The researchers also used mouse models to uncover how this molecule interacts with genes involved in inflammation and tissue regeneration. In mice lacking SNHG26, wound healing was delayed, emphasising the molecule’s importance in the balance between inflammation and tissue repair. The discovery paves the way for new therapeutic approaches for acute and chronic wounds.

Single-cell transcriptomic analysis of impaired wound repair in Snhg26-KO mice

Fig. 3

a UMAP plot and cluster annotation of 21491 cells from skin and wounds of Snhg26-KO and WT mice (n = 3/group). b UMAP plot showing the expression of Snhg26 in Snhg26-KO and WT mice. c Violin plot showing the expression of Snhg26 in different cell types in WT mice. d Comparison of skin and wound cell composition between the KO and WT mice. Red line indicates keratinocyte clusters with changed cell composition in the wound of KO mice. Blue line indicates immune cell clusters. e The proportion of DEGs [log2(FC) ≥ 0.3, -log10(FDR) > 2] within all expressed genes in individual cell clusters in wounds of Snhg26-KO and WT mice. f GO and KEGG analysis of the top 200 marker genes in basal keratinocyte cell clusters. g The proliferation, migration, and inflammatory scores were plotted for each keratinocyte cluster. h–j Violin plots showing keratinocyte migration (h), proliferation (i) and inflammation scores (j) in Snhg26-KO and WT mice wound basal keratinocytes. k Circle plots displaying the CCL signaling network in Snhg26-KO and WT mice wounds. The changed signals in the KO mice compared to the WT mice were highlighted with arrows. The data were analyzed by two- sided post hoc test (c), two- sided Fisher’s exact test (f) or two-sided Mann-Whitney U test (h–j).

“By targeting SNHG26, we may be able to accelerate healing and reduce complications, particularly in chronic wounds where prolonged inflammation is a major problem,” says Ning Xu Landén.

Also studies microRNA

Her research group at Karolinska Institutet is studying how healing processes in the skin are controlled by so-called regulatory RNA molecules, i.e. RNA molecules that regulate gene activity and include both lncRNAs and the now Nobel Prize-awarded microRNA molecules. The researchers will now continue to study how other regulatory RNA molecules are involved in tissue repair, with the aim of developing innovative treatments for hard-to-heal wounds

Source – Karolinska Institutet

Li D, Liu Z, Zhang L, Bian X, Wu J, Li L, Chen Y, Luo L, Pan L, Kong L, Xiao Y, Wang J, Zhang X, Wang W, Toma M, Piipponen M, Sommar P, Xu Landén N. (2024) The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healing. Nat Commun 15(1):8637. [article]

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