Prostaglandin E2 Affects Proliferation and Collagen Synthesis by Human Patellar Tendon Fibroblasts

Abstract

Based on these in vitro findings, we speculate that production of prostaglandin E2 in tendons might play some role in the acellularity and matrix disorganization seen in exercise-induced tendinopathy.

Leukotriene B4 at low dosage negates the catabolic effect of prostaglandin E2 in human patellar tendon fibroblasts

“…This study also showed that PGE 2 at 100 ng/ml significantly decreased HPTF proliferation, which is consistent with the result of our previous report (Cilli et al, 2004). Furthermore, low concentrations (≤1 nM) of LTB 4 negated the inhibitory effect of PGE 2 on HPTF proliferation.…”

“…6). These results suggest that PGE 2 -mediated inhibition of collagen production, as shown in our previous study (Cilli et al, 2004), is perhaps via the induction of collagen-degrading enzymes such as MMP-1 and MMP-3. Another possibility for the decrease in collagen production by PGE 2 is that PGE 2 affects collagen mRNA stability.…”

“…After 24 h, varying concentrations of LTB 4 (Cayman Chemicals, Ann Arbor, Michigan), ranging from 10 pM to 10 nM, were added to the wells. PGE 2 was added to the cell cultures at a dose of 100 ng/ml because our previous study showed that this PGE 2 dose decreases HPTF proliferation and collagen production (Cilli et al, 2004). Fibroblasts treated with EtOH (0.1%), which is the vehicle for PGE 2 or LTB 4 , were used as the control groups.…”

“…In addition, elevated PGE 2 levels were found in the human tendon after repetitive mechanical loading (Langberg et al, 1999). Recently, we have shown that exogenous addition of PGE 2 at a dose of 100 ng/ml decreases proliferation and collagen production in human patellar tendon fibroblasts (HPTFs) (Cilli et al, 2004). On the other hand, LTB 4 at picomolar concentrations has been shown to stimulate DNA synthesis in cultured human epidermal keratinocytes and to induce proliferation of arterial smooth muscle cells in primary culture (Kragballe et al, 1985;Palmberg et al, 1989).…”

The Achilles Tendinopathy: Pathogenesis Review

“…The results of the increased levels of VEGF in tendons are mainly two: on the one hand the alteration of the tendon matrix which leads to a weakening of the tendon structure; on the other hand the following nervous ingrowth that causes pain symptoms. It was recently shown that human tendon increase in proliferation (as well as gene expression and type I collagen production) in a stretching magnitude-dependent manner [112] ; overload, on the opposite, can decrease proliferation and collagen production in human tendon fibroblasts, changing the extracellular matrix composition and even resulting in tenocytes apoptosis (programmed cell death) [113][114][115] . Since tenocytes are required to maintain homeostasis of the extracellular matrix (ECM) by regulating the balance between its synthesis and degradation [116] , tenocyte apoptosis may compromise the ability of the tendon to regulate repair processes.…”