Research group Mona Ståhle
Research group Mona Ståhle
The research comprises several core areas in dermatology and the main long-term projects include comprehensive genetic epidemiologic studies in chronic inflammatory skin diseases, basic preclinical research on skin barrier structure and function, skin cancer and UV-related skin diseases.
Mona Ståhle Group leader
Enikö Pivarcsi Sonkoly
Ning Xu Landén
Kunal Das MahapatraPhD student
Lorenzo PasqualiPhD student, Graduate Student
Heshuang QuGraduate Student
Enikö SonkolySenior lecturer/specialist physician
Ankit SrivastavaPhD student
Mona StåhleProfessor, senior
Axel SvedbomPhD student, Graduate Student
Jakob WikströmAssistant professor
Anna-Maria WintlerGraduate Student
The projects directly supervised within my own team include two main areas, Psoriasis and Wound healing. Within these two blocks several independent but connected projects have formed. Our research is based on a fusion between clinical work at Hudkliniken Karolinska universitetssjukhuset, Solna and experimental work performed at Molecular Dermatology , CMM, Karolinska universitetssjukhuset, Solna.
Psoriasis - epidemiology, genetics and biology
Our research is part of the Karolinska Psoriasis Center which is the clinical base for treatment of psoriasis patients who need systemic treatments to control their disease. A clinical trial unit undertaking Phase II and III trials is affiliated. The laboratory where the experimental preclinical research is based is located at CMM in close vicinity to the clinical facilities. The psoriasis team includes in addition to clinicians, senior scientists, post-docs , graduate students and nurses. Several team members share their time between the laboratory and the clinic which enables a truly translational approach.
Psoriasis is a common and complex inflammatory skin disease with significant co-morbidity. The genetic basis for psoriasis is strong. Clinical heterogeneity suggests that different subtypes have distinct genetic background and respond differently to treatment. In 2000 we started a cohort of adult psoriasis patients recruited at the onset of disease, Stockholm Psoriasis Cohort (SPC). Today SPC includes close to 800 cases with an equal number of matched controls. In this project we have described clinical characteristics and triggering factors at disease onset and co-morbidities with focus on the metabolic profile and cardiovascular overrisk associated with psoriasis. The SPC cohort represents a cross-section of all phenotypes with the majority of cases being mild. A 10 year follow up will commence in 2011 which will provide valuable information on the natural disease course and development. To complement the SPC, we also study patients with severe psoriasis who receive systemic treatment and we have established a biobank from these patients with the aim to identify biomarkers for treatment response and genotype/phenotype profiles. Childhood psoriasis representing a distinct subphenotype is another interest. In addition to genetic susceptibility factors, we study inflammatory pathways during different disease phases and the putative role of microRNAs and their targets which are diffentially expressed in psoriasis.
Wound healing is a fundamental biologic process that entails a complex coordination of inflammation, cell migration, proliferation and tissue remodelling. How this physiologic process is controlled and executed is still insufficiently understood and mechanisms leading to impaired wound healing and chronic ulcers even less.
For the past few years we have focused on the role of the human cathelicidine protein , hCAP18/LL-37 in this process. We have shown that hCAP18/LL-37 is lacking in chronic ulcers and is upregulated during normal physiologic wound healing. The project is at present focused on studying molecular pathways involved in hCAP18 signaling and its role in cell migration and proliferation. One aim of this project is to develop treatments for impaired wound healing.
MicroRNA-125b down-regulates matrix metallopeptidase 13 and inhibits cutaneous squamous cell carcinoma cell proliferation, migration, and invasion.
Xu N, Zhang L, Meisgen F, Harada M, Heilborn J, Homey B, et al
J. Biol. Chem. 2012 Aug;287(35):29899-908
Genetic association with ERAP1 in psoriasis is confined to disease onset after puberty and not dependent on HLA-C*06.
Lysell J, Padyukov L, Kockum I, Nikamo P, Ståhle M
J. Invest. Dermatol. 2013 Feb;133(2):411-7
Cost-effective HLA-Cw06:02 typing in a Caucasian population.
Nikamo P, Ståhle M
Exp. Dermatol. 2012 Mar;21(3):221-3
Identification of the cathelicidin peptide LL-37 as agonist for the type I insulin-like growth factor receptor.
Girnita A, Zheng H, Grönberg A, Girnita L, Ståhle M
Oncogene 2012 Jan;31(3):352-65