NING XU LANDÉN GROUP
MicroRNA and wound healing
Both chronic non-healing wounds and psoriasis are major and rising health and economic burdens worldwide and lack of effective treatment. Investigation of the role of regulatory RNAs, for example microRNA and long non-coding RNAs, represents an emerging concept, and constitutes a promising area for pharmaceutical intervention. The goal of our laboratory is to unravel the role(s) of regulatory RNAs in skin wound healing and in psoriasis. Moreover, we aim to translate basic scientific findings into therapeutic interventions for patients.
Project 1. The role of non-coding RNAs in human skin wound healing
The goal of our research is to develop novel RNA-based treatments to improve healing of human skin wounds. The immense economic and social impact of deficient wound healing e.g. chronic ulcers post-surgical wounds care and skin scarring, calls for attention and allocation of resources to understand biological mechanisms underlying wound complications. Due to the complex nature of wounds, efficient targeted approach to enhance healing are essentially lacking today.
The recent discovery of non-coding RNAs (ncRNAs) as powerful gene regulators provides hope to develop novel RNA-based treatments for a wide variety of diseases. However, the role of ncRNAs in human skin wound healing remains largely unexplored.
The objective of our study is to reveal the role(s) of ncRNAs in skin wound healing and to explore the potential of RNA-based therapy for chronic wounds. We primarily focus on small ncRNAs, i.e. microRNAs (miRNAs) and long-non-coding RNAs (lncRNAs) and study:
(i) The expression profiles of miRNA/lncRNA in injured human skin;
(ii) The biological function of differentially expressed miRNAs/lncRNAs in wounds;
(iii) The molecular mechanisms mediating the biological functions of wound related miRNAs/lncRNAs;
(iv) The therapeutic potentials of targeting wound related miRNAs.
Our research network is composed of both clinicians and scientists, which allows us to perform ‘Bench-to-Bedside’ research. At present, we are investigating the novel roles of miRNAs and lncRNAs in skin wounds using our unique collection of human wound tissues. In the next step, we aim to translate our basic scientific findings into therapeutic interventions for wound patients.
Project 2. Investigation of the mechanistic links between psoriasis and co-morbidities
Psoriasis is an immune-mediated inflammatory disease of the skin. It is a lifelong disease with spontaneous remissions and exacerbations, affecting the patients’ life quality substantially, and there is no cure for it today. Epidemiological studies show that psoriasis patients have increased risks of developing systemic co-morbidities, e.g. obesity, overt diabetes and cardiovascular disease; however, the molecular mechanisms behind these co-morbidities remain unexplored. We have previously demonstrated that miRNAs play important roles in skin inflammation of psoriasis. Here, we study whether miRNA could also be a key mechanistic link between psoriasis and its co-morbidities, using materials from a large biobank of psoriasis patients in Stockholm. This study will further increase our understanding about pathogenesis of psoriasis. It is essential for the effective management of psoriasis and prevention of its related co-morbidities.
Lau grant from the Ming Wai Lau Centre for Reparative Medicine
Ragnar Söderbergs Foundation
Swedish Research Council (project and network grants)
Swedish Psoriasis Foundation
Åke wibergs Foundation
HudFonden (Swedish dermatology foundation)
KI Faculty funded position as senior researcher
Karolinska Institutet KID-grant
Karolinska Institute foundation
Foundation La Roche-Posay
Swedish medical doctor society (SLS) research fund
European Skin Research Foundation
Swedish society for medical research (SSMF) fund
Pfizer AB Investigator Initiated Research fund
Tore Nilssons foundation for medical research
Lars Hiertas memorial foundation
Sigurt och Elsa Goljes memorial foundation
We always want to get in touch with talented potential co-workers. If you are interested in doing research within our group, as a degree project or as a researcher, please contact Ning (email@example.com). We would also be happy to help with applications for external support for PhD study or postdoctoral fellowships.
We organize the following doctoral course at KI
In situ hybridization: theory and practice (#2872)
Find a link to KI doctoral courses:
Master’s and other projects:
We are always looking for talented and interested students.
Link to all publications on PubMed.
Li X, Li D, Wang A, Chu T, Lohcharoenkal W, Zheng X, Grünler J, Narayanan S, Eliasson S, Herter E, Wang Y, Ma Y, Ehrström M, Eidsmo L, Pivarcsi A, Sonkoly E, Catrina S, Ståhle M, Xu Landén N. MicroRNA-132 with therapeutic potential in chronic wounds. J Invest Dermatol. 2017 Dec;137(12):2630-2638.
Li X, Li D, Wikström J.D., Pivarcsi A, Sonkoly E, Ståhle M, Xu Landén N. MicroRNA-132 promotes fibroblast migration via regulating RAS p21 protein activator 1 in skin wound healing. Sci Rep. 2017 Aug 10;7(1):7797.
Herter EK, Landén NX. Non-coding RNAs: new players in skin wound healing. Advances in Wound Care. 2017 Mar 1;6(3):93-107.
Landén NX, Li D, Ståhle M. Transition from inflammation to proliferation: a critical step during wound healing. Cell Mol Life Sci. 2016 Oct;73(20):3861-85.
Cheung L, Fisher RM, Kuzmina N, Li D, Li X, Werngren O, Blomqvist L, Ståhle M, Landén NX. Psoriasis skin inflammation-induced microRNA-26b targets NCEH1 in underlying subcutaneous adipose tissue. J Invest Dermatol. 2016 Mar;136(3):640-648.
Li D, Wang A, Liu X, Meisgen F, Grunler J, Botusan IR, Narayanan S, Erikci E, Li X, Blomqvist L, Du L, Pivarcsi A, Sonkoly E, Chowdhury K, Catrina S, Ståhle M, Landén NX. MicroRNA-132 enhances transition from inflammation to proliferation during wound healing. J Clin Invest. 2015 Aug 3;125(8):3008-26.
Li D, Wang A, Meisgen F, Pivarcsi A, Sonkoly E, Ståhle M, Landén NX. MicroRNA-31 promotes skin wound healing by enhancing keratinocyte proliferation and migration. J Invest Dermatol. 2015 Jun;135(6):1676-1685.