Τίτλος:
Mitochondrial dysfunction in affected skin and increased mitochondrial
DNA in serum from patients with psoriasis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Psoriasis is characterized by keratinocyte proliferation and chronic
inflammation, but the pathogenesis is still unclear. Dysregulated
mitochondria (mt) could lead to reduced apoptosis and extracellular
secretion of mtDNA, acting as “innate pathogen” triggering
inflammation. Serum was obtained from healthy volunteers and psoriatic
patients. Mitochondrial DNA was extracted from the serum and amplified
with quantitative PCR (qPCR). Punch biopsies were obtained from lesional
and non-lesional psoriatic skin (10 cm apart) and from healthy
volunteers, were placed in RNA later and were stored at -80 degrees C
until RNA was extracted and cDNA was synthesized; gene expression of
uncoupling protein 2 (UCP2), Dynamin-related protein 1 (Drp1) and
calcineurin, involved in the regulation of mitochondria function, was
detected with qPCR. Mitochondrial DNA was significantly increased (7s, P
= 0.0496 and Cytochrome B, CytB, P = 0.0403) in the serum of psoriatic
patients (n = 63) as compared to controls (n = 27). Gene expression was
significantly reduced for UCP2 (P = 0.0218), Drp1 (P = 0.0001) and
calcineurin (P = 0.0001) in lesional psoriatic skin, as compared to
non-lesional or control skin. Increased serum extracellular mtDNA in
psoriatic patients and decreased expression of mitochondrial regulatory
proteins in psoriatic skin suggest increased inflammation and reduced
keratinocyte apoptosis, respectively. Inhibitors of mtDNA secretion
and/or UCP2 stimulants may be potential treatment options.
Συγγραφείς:
Therianou, Anastasia
Vasiadi, Magdalini
Delivanis, Danae A. and
Petrakopoulou, Theodora
Katsarou-Katsari, Alexandra
Antoniou,
Christina
Stratigos, Alexandros
Tsilioni, Irene
Katsambas,
Andreas
Rigopoulos, Dimitris
Theoharides, Theoharis C.
Περιοδικό:
CLINICAL AND EXPERIMENTAL DERMATOLOGY
Λέξεις-κλειδιά:
apoptosis; calcineurin; DNA; Drp1; inflammation; mitochondria;
psoriasis; UCP2
