Streptozotocin-induced diabetes alters transcription of multiple genes necessary for extracellular matrix remodeling in rat patellar tendon.
Connect Tissue Res
; 59(5): 447-457, 2018 09.
Article
en En
| MEDLINE
| ID: mdl-29745261
OVERVIEW: Tendon collagen fibril degradation is commonly seen in tendons of diabetics, but the mechanisms responsible for these changes remain to be elucidated. We have demonstrated that streptozotocin (STZ)-induced diabetes increases tendon cell proliferation and collagen content. In the present study, we evaluated that impact of STZ-induced diabetes on mRNA transcripts involved with collagen fibril organization, extracellular matrix (ECM) remodeling, apoptosis, and proliferation. MATERIALS AND METHODS: Rats were divided into four groups: nondiabetic (control, n = 9), 1 week (acute, n = 8) or 10 weeks of diabetes (chronic, n = 7), and 10 weeks of diabetes with insulin (insulin, n = 8). RNA was isolated from the patellar tendon for determination of mRNA transcripts using droplet digital PCR (ddPCR). RESULTS: Transcripts for Col1a1, Col3a1, Mmp2, Timp1, Scx, Tnmd, Casp3, Casp8, and Ager were lower in acute relative to control and insulin rats (p ≤ 0.05). With the exception of Scx, transcripts for Col1a1, Col3a1, Mmp2, Timp1, Tnmd, Casp3, Casp8, and Ager were also lower in chronic when compared to control (p < 0.05). Transcripts for Col1a1, Col3a1, Mmp2, Timp1, Tnmd, Casp3, Casp8, and Ager were not different between control and insulin (p > 0.05). Transcripts for Dcn, Mmp1a, Mmp9, Pcna, Tgfbr3, Ptgs2, Ptger2, Ptges, and iNos were not altered by diabetes or insulin (p > 0.05). CONCLUSION: Our findings indicated that STZ-induced diabetes results in rapid and large changes in the expression of several genes that are key to ECM remodeling, maintenance, and maturation.
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Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Transcripción Genética
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Ligamento Rotuliano
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Diabetes Mellitus Experimental
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Matriz Extracelular
Límite:
Animals
Idioma:
En
Revista:
Connect Tissue Res
Año:
2018
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Reino Unido