Alteration in Gene Expression of STAT4 and PIAS2 in Individuals with Type 2 Diabetes Mellitus Treated with the Dipeptidyl Peptidase 4 Inhibitor

Sina Nabiyi; Firozeh Sajedi; Alireza Zamani; Mahdi Behzad

Makale detayları

Alteration in Gene Expression of STAT4 and PIAS2 in Individuals with Type 2 Diabetes Mellitus Treated with the Dipeptidyl Peptidase 4 Inhibitor

Yazarlar:

Sina Nabiyi | Firozeh Sajedi | Alireza Zamani | Mahdi Behzad

Yayıncı:

Istanbul University

Ana Başlıklar:

Clinical Sciences (Other)

Dergi:

Experimed Vol.13 Issue 3, pp.163-169

Belge Tipi:

Makale

Yayın Tarihi:

12/2023

Belge Dili:

İngilizce

Document ID (Org No.):

2001310803

pISSN:

2667-5846

Anahtar kelimeler:

Özet:

 Objective: Impairment of immune cell signaling molecules is involved in diseases pathogenesis. The evaluation of signal transducer and activator of transcription STAT 4 and protein inhibitor of activated STAT PIAS 2 as well as immunoregulatory role of the dipeptidyl peptidase-4 inhibitor, sitagliptin were investigated in type 2 diabetes mellitus T2DM. Materials and Methods: Peripheral blood mononuclear cells were purified from three study groups including healthy controls, T2DM patients with 6 months of sitagliptin treatment, and T2DM patients without sitagliptin. Expressions of STAT4 and PIAS2 were assessed with real-time polymerase chain reaction qPCR. Results: The expression of STAT4 in patients without sitagliptin was higher than the healthy controls p0.001. Its expression was down-regulated in the sitagliptin treated patient group compared to those without sitagliptin p0.005. PIAS2 expression in patients without sitagliptin was lower than the healthy controls p0.009. PIAS2 was elevated in the sitagliptin treated group versus patients without sitagliptin p0.003. A negative correlation between STAT4 and PIAS2 was found in individuals without sitagliptin p0.01. In patients without sitagliptin, fasting plasma glucose was positively and negatively correlated with STAT4 and PIAS2, respectively p0.004 and p0.001. Conclusion: Aberrant expression of STAT4 and reduced expression of PIAS2 were found in the T2DM patients. Sitagliptin may regulate the cell signaling pathways by elevating PIAS2 and reducing STAT4.

 Objective: Impairment of immune cell signaling molecules is involved in diseases pathogenesis. The evaluation of signal transducer and activator of transcription STAT 4 and protein inhibitor of activated STAT PIAS 2 as well as immunoregulatory role of the dipeptidyl peptidase-4 inhibitor, sitagliptin were investigated in type 2 diabetes mellitus T2DM. Materials and Methods: Peripheral blood mononuclear cells were purified from three study groups including healthy controls, T2DM patients with 6 months of sitagliptin treatment, and T2DM patients without sitagliptin. Expressions of STAT4 and PIAS2 were assessed with real-time polymerase chain reaction qPCR. Results: The expression of STAT4 in patients without sitagliptin was higher than the healthy controls p0.001. Its expression was down-regulated in the sitagliptin treated patient group compared to those without sitagliptin p0.005. PIAS2 expression in patients without sitagliptin was lower than the healthy controls p0.009. PIAS2 was elevated in the sitagliptin treated group versus patients without sitagliptin p0.003. A negative correlation between STAT4 and PIAS2 was found in individuals without sitagliptin p0.01. In patients without sitagliptin, fasting plasma glucose was positively and negatively correlated with STAT4 and PIAS2, respectively p0.004 and p0.001. Conclusion: Aberrant expression of STAT4 and reduced expression of PIAS2 were found in the T2DM patients. Sitagliptin may regulate the cell signaling pathways by elevating PIAS2 and reducing STAT4.

 Objective: Impairment of immune cell signaling molecules is involved in diseases pathogenesis. The evaluation of signal transducer and activator of transcription STAT 4 and protein inhibitor of activated STAT PIAS 2 as well as immunoregulatory role of the dipeptidyl peptidase-4 inhibitor, sitagliptin were investigated in type 2 diabetes mellitus T2DM. Materials and Methods: Peripheral blood mononuclear cells were purified from three study groups including healthy controls, T2DM patients with 6 months of sitagliptin treatment, and T2DM patients without sitagliptin. Expressions of STAT4 and PIAS2 were assessed with real-time polymerase chain reaction qPCR. Results: The expression of STAT4 in patients without sitagliptin was higher than the healthy controls p0.001. Its expression was down-regulated in the sitagliptin treated patient group compared to those without sitagliptin p0.005. PIAS2 expression in patients without sitagliptin was lower than the healthy controls p0.009. PIAS2 was elevated in the sitagliptin treated group versus patients without sitagliptin p0.003. A negative correlation between STAT4 and PIAS2 was found in individuals without sitagliptin p0.01. In patients without sitagliptin, fasting plasma glucose was positively and negatively correlated with STAT4 and PIAS2, respectively p0.004 and p0.001. Conclusion: Aberrant expression of STAT4 and reduced expression of PIAS2 were found in the T2DM patients. Sitagliptin may regulate the cell signaling pathways by elevating PIAS2 and reducing STAT4.

 Objective: Impairment of immune cell signaling molecules is involved in diseases pathogenesis. The evaluation of signal transducer and activator of transcription STAT 4 and protein inhibitor of activated STAT PIAS 2 as well as immunoregulatory role of the dipeptidyl peptidase-4 inhibitor, sitagliptin were investigated in type 2 diabetes mellitus T2DM. Materials and Methods: Peripheral blood mononuclear cells were purified from three study groups including healthy controls, T2DM patients with 6 months of sitagliptin treatment, and T2DM patients without sitagliptin. Expressions of STAT4 and PIAS2 were assessed with real-time polymerase chain reaction qPCR. Results: The expression of STAT4 in patients without sitagliptin was higher than the healthy controls p0.001. Its expression was down-regulated in the sitagliptin treated patient group compared to those without sitagliptin p0.005. PIAS2 expression in patients without sitagliptin was lower than the healthy controls p0.009. PIAS2 was elevated in the sitagliptin treated group versus patients without sitagliptin p0.003. A negative correlation between STAT4 and PIAS2 was found in individuals without sitagliptin p0.01. In patients without sitagliptin, fasting plasma glucose was positively and negatively correlated with STAT4 and PIAS2, respectively p0.004 and p0.001. Conclusion: Aberrant expression of STAT4 and reduced expression of PIAS2 were found in the T2DM patients. Sitagliptin may regulate the cell signaling pathways by elevating PIAS2 and reducing STAT4.

Makale detayları

Alteration in Gene Expression of STAT4 and PIAS2 in Individuals with Type 2 Diabetes Mellitus Treated with the Dipeptidyl Peptidase 4 Inhibitor

Yazarlar:

Sina Nabiyi | Firozeh Sajedi | Alireza Zamani | Mahdi Behzad

Yayıncı:

Istanbul University

Ana Başlıklar:

Clinical Sciences (Other)

Dergi:

Experimed Vol.13 Issue 3, pp.163-169

Belge Tipi:

Makale

Yayın Tarihi:

12/2023

Belge Dili:

İngilizce

Document ID (Org No.):

2001310803

pISSN:

2667-5846

Type 2 diabetes mellitus

STAT

PIAS

dipeptidyl peptidase 4 inhibitor

Sayı

Makale detayları

Alteration in Gene Expression of STAT4 and PIAS2 in Individuals with Type 2 Diabetes Mellitus Treated with the Dipeptidyl Peptidase 4 Inhibitor

Yazarlar: Sina Nabiyi | Firozeh Sajedi | Alireza Zamani | Mahdi Behzad

Yayıncı: Istanbul University

Ana Başlıklar: Clinical Sciences (Other)

Dergi: Experimed Vol.13 Issue 3, pp.163-169

Belge Tipi: Makale

Yayın Tarihi: 12/2023

Belge Dili: İngilizce

Document ID (Org No.): 2001310803

pISSN: 2667-5846

Type 2 diabetes mellitus

STAT

PIAS

dipeptidyl peptidase 4 inhibitor

Sayı

Yazarlar:

Sina Nabiyi | Firozeh Sajedi | Alireza Zamani | Mahdi Behzad

Yayıncı:

Istanbul University

Ana Başlıklar:

Clinical Sciences (Other)

Dergi:

Experimed Vol.13 Issue 3, pp.163-169

Belge Tipi:

Makale

Yayın Tarihi:

12/2023

Belge Dili:

İngilizce

Document ID (Org No.):

2001310803

pISSN:

2667-5846