Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment
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ORIGINAL ARTICLE
Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment G. Ruiz-Heiland 1
&
J. W. Yong 1 & J. von Bremen 1 & S. Ruf 1
Received: 13 January 2020 / Accepted: 5 August 2020 # The Author(s) 2020
Abstract Objectives Juvenile obesity is a complex clinical condition that is present more and more frequently in the daily orthodontic practice. Over-weighted patients have an impaired bone metabolism, due in part to their increased levels of circulating adipokines. Particularly, leptin has been reported to play a key role in bone physiology. Leptin is ubiquitously present in the body, including blood, saliva, and crevicular fluid. If, and to what extent, it could influence the reaction of cementoblasts during orthodontic-induced forces is yet unknown. Material and methods OCCM-30 cementoblasts were cultivated under compressive forces using different concentrations of leptin. The expression of ObR, Runx-2, Osteocalcin, Rank-L, Sost, Caspase 3, 8, and 9 were analyzed by RT-PCR. Western blots were employed for protein analysis. The ERK1/2 antagonist FR180204 (Calbiochem) was used and cPLA2 activation, PGE2, and cytochrome C release were further evaluated. Results In vitro, when compressive forces are applied, leptin promotes ERK1/2 phosphorylation, as well as upregulates PGE2 and caspase 3 and caspase 9 on OCCM cells. Blockade of ERK1/2 impairs leptin-induced PGE2 secretion and reduced caspase 3 and caspase 9 expression. Conclusions Leptin influences the physiological effect of compressive forces on cementoblasts, exerting in vitro a proinflammatory and pro-apoptotic effect. Clinical relevance Our findings indicate that leptin exacerbates the physiological effect of compressive forces on cementoblasts promoting the release of PGE2 and increases the rate of cell apoptosis, and thus, increased levels of leptin may influence the inflammatory response during orthodontically induced tooth movement. Keywords Cementoblasts . ERK1/2 . Leptin
Introduction In all age groups, the prevalence of obesity has been increasing worldwide over the last decades. It is well known that obesity is an important risk factor for many chronic diseases (WHO) [1]. Due to the excess of adipose tissue, the number and volume of adipocytes are increased. Adipocytes are a highly active endocrine organ which produces and releases a variety of adipokines, in particular, increased amounts of proinflammtory adipokines, such as leptin, and decreased amounts of anti-inflammatory
* G. Ruiz-Heiland [email protected] 1
Department of Orthodontics, University of Giessen, Schlangenzahl 14, 35392, Giessen, Germany
adipokines, such as adiponectin. This imbalance between proand anti-inflammatory adipokines results in a subclinical chronic systemic inflammation status of obese patients [2–4]. Being the first adipokine discovered, leptin has attracted special research interest [5]. In general medicine, higher leptin levels have been associated with several chronic
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