Functional cross-talk of integrin b3 and AP-1 in differentiating osteoclasts and dendritic cells.

VAŇHARA, Petr, Kateřina SKÁLOVÁ, Eva ONDROUŠKOVÁ a Jan ŠMARDA. Functional cross-talk of integrin b3 and AP-1 in differentiating osteoclasts and dendritic cells. In Book of Abstracts. Warsaw: International Life Sciences Students's Conference, 2008, 2 s. ISBN 978-83-927731-0-8.

Základní údaje

• Originální název: Functional cross-talk of integrin b3 and AP-1 in differentiating osteoclasts and dendritic cells.
• Název česky: Funkční interakce integrinu beta 3 a AP-1 v diferencujících osteoklastech a dendritických buňkách
• Autoři: VAŇHARA, Petr (203 Česká republika), Kateřina SKÁLOVÁ (203 Česká republika), Eva ONDROUŠKOVÁ (203 Česká republika) a Jan ŠMARDA (203 Česká republika, garant).
• Vydání: Warsaw, Book of Abstracts, 2 s. 2008.
• Nakladatel: International Life Sciences Students's Conference

Další údaje

• Originální jazyk: angličtina
• Typ výsledku: Stať ve sborníku
• Obor: Genetika a molekulární biologie
• Stát vydavatele: Polsko
• Utajení: není předmětem státního či obchodního tajemství
• Kód RIV: RIV/00216224:14110/08:00024909
• Organizační jednotka: Lékařská fakulta
• ISBN: 978-83-927731-0-8
• Klíčová slova anglicky: osteoclasts; dendritic cells; integrin beta 3; AP-1
• Štítky: AP-1, dendritic cells, integrin beta 3, osteoclasts
• Příznaky: Mezinárodní význam, Recenzováno

Anotace

Osteoclasts (OCL) and dendritic cells (DC) are highly specialized cells that originate from a common hematopoetic progenitor. The osteoclasts are involved in bone resorption; dendritic cells represent a key compound of immune system as antigen presenting cells. Despite distinct functions, similar signaling molecules are involved in control of differentiation of OCL and DC. These regulators include integrin b3, the ECM receptor, and transcription factors c-Jun and c-Fos (AP-1). To investigate the signaling crosstalk between Itgb3 and AP-1 in OCL and DC, we employed murine model of RAW264.7 macrophages. These cells differentiate to OCL or DC upon treatment with RANKL (Receptor activator of NFkB ligand)MCSF or LPS (Lipopolysacharide). Expression of itgb3, c-jun and c-fos as well as differentiation markers were determined at mRNA level by qRT-PCR or western blotting. Expression of itgb3 was induced by both RANKL MCSF and LPS; however, expression of c-fos and c-jun was regulated differently in DC and OCL. Peptides containing Arg-Gly-Asp (RGD) sequence activate Itgb3 pathway specifically and induce expression of c-jun, c-fos and itgb3 in OCL but not in DC upon treatment with LPS. Similarly, inhibition of AP-1 by Jun N terminal kinase inhibitor (JNKi) increases expression of c-fos and itgb3, however it leaves expression of c-jun unaffected upon treatment with MCSF-RANKL or LPS. Moreover, JNKi, but not RGD, completely inhibits the M-CSF/RANKL-induced differentiation of RAW 264.7 cells to OCL and DC. We presume that there is mutual positive regulation between Itgb3- and c-Jun and c-Fos expression in OCL and DC.

Anotace česky

Osteoclasts (OCL) and dendritic cells (DC) are highly specialized cells that originate from a common hematopoetic progenitor. The osteoclasts are involved in bone resorption; dendritic cells represent a key compound of immune system as antigen presenting cells. Despite distinct functions, similar signaling molecules are involved in control of differentiation of OCL and DC. These regulators include integrin b3, the ECM receptor, and transcription factors c-Jun and c-Fos (AP-1). To investigate the signaling crosstalk between Itgb3 and AP-1 in OCL and DC, we employed murine model of RAW264.7 macrophages. These cells differentiate to OCL or DC upon treatment with RANKL (Receptor activator of NFkB ligand)MCSF or LPS (Lipopolysacharide). Expression of itgb3, c-jun and c-fos as well as differentiation markers were determined at mRNA level by qRT-PCR or western blotting. Expression of itgb3 was induced by both RANKL MCSF and LPS; however, expression of c-fos and c-jun was regulated differently in DC and OCL. Peptides containing Arg-Gly-Asp (RGD) sequence activate Itgb3 pathway specifically and induce expression of c-jun, c-fos and itgb3 in OCL but not in DC upon treatment with LPS. Similarly, inhibition of AP-1 by Jun N terminal kinase inhibitor (JNKi) increases expression of c-fos and itgb3, however it leaves expression of c-jun unaffected upon treatment with MCSF-RANKL or LPS. Moreover, JNKi, but not RGD, completely inhibits the M-CSF/RANKL-induced differentiation of RAW 264.7 cells to OCL and DC. We presume that there is mutual positive regulation between Itgb3- and c-Jun and c-Fos expression in OCL and DC.

Návaznosti

• GA301/06/0036, projekt VaV: Název: Úloha vybraných transkripčních faktorů v osteoklastové diferenciační dráze

Investor: Grantová agentura ČR, Úloha vybraných transkripčních faktorů v osteoklastové diferenciační dráze

• GD204/08/H054, projekt VaV: Název: Molekulární mechanismy proliferace a diferenciace buněk

Investor: Grantová agentura ČR, Molekulární mechanismy proliferace a diferenciace buněk

• MSM0021622415, záměr: Název: Molekulární podstata buněčných a tkáňových regulací

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Molekulární podstata buněčných a tkáňových regulací