Naslov
TRP channels overexpression contributes to in ammasome activation in clavicular cortical hyperostosis?

Autori
Lamot, Lovro ; Vidović, Mandica ; Perica, Marija ; Tambić Bukovac, Lana ; Gotovac, Kristina ; Borovečki, Fran ; Harjaček, Miroslav

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Skup
4th Congress of Immunology

Mjesto i datum
Beč, Austrija, 06.09.2016. - 09.09.2016

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Clavicular cortical hyperostosis; CCH; CRMO; chronic reccurent multifocal osteomyelitis; microarray

Sažetak
Background: Clavicular cortical hyperostosis (CCH) is a sterile in ammatory bone disorder of unknown etiology clinically characterized by pain and/or swelling of the clavicle. Objectives: Identi cation of speci c gene expression patterns in CCH patients. Methods: Total RNA was isolated from whole blood of 18 new-onset, untreated CCH patients and 8 healthy controls. DNA microarray gene expression was preformed in 5 CCH and 4 control patients along with bioinformatical analysis of retrieved data. Carefully selected di erentially expressed genes where analyzed by qRT-PCR in all participants of the study. Results: Microarray results and bioinformatical analysis revealed 974 di erentially expressed genes involved in various in ammatory processes, while qRT-PCR analysis showed signi cantly higher expression of TRPM3 and TRPM7, as well as lower expression of ERBB2. Conclusions: TRPM3 and TRPM7 are transient receptor potential (TRP) proteins that act as multimodal sensor cation channels for a wide variety of stimuli, one of which is environmental temperature that in the case of CCH could be elicited by overuse of sterno- clavicular joint (SCJ). Altered TRP channel function can have strong e ects on a variety of cellular and systemic processes, including the activation and the regulation of the in ammasomes. ERBB2 belongs to a family of genes that encodes for cell surface growth factor receptors. ErbB activation promotes protective cellular outcomes during in ammation, hence lower expression of this gene could cause damage due to in ammation. We hypothesize that CCH could be an autoin ammatory disease induced by SCJ overuse, TRP channel overexpression, in ammasome activation and reduced protection during in ammation.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti

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