Prolactin inhibits the apoptosis of chondrocytes induced by serum starvation

Zermeño, C; Guzmán-Morales, Jessica; Macotela, Yazmín; Nava, Gabriel Miranda; López-Barrera, Fernándo; Kourí, Juan B.; Lavalle, C; Escalera, Gonzálo Martínez de la; Clapp, Carmen

doi:10.1677/joe.1.06766

Cited by 24 publications

(23 citation statements)

References 40 publications

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“…PRL and the PRL receptor are expressed in chondrocytes (12,13), where this hormone can promote differentiation and survival. PRL stimulates the synthesis of proteoglycans and type II collagen by bone marrow-derived chondrocytic mesenchymal cells (14), and it inhibits the apoptosis of articular chondrocytes induced by serum deprivation (13). The action of PRL on chondrocyte survival may be relevant in RA.…”

Section: Introductionmentioning

confidence: 99%

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

et al. 2013

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Chondrocytes are the only cells in cartilage, and their death by apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA). A putative therapeutic intervention for RA is the inhibition of apoptosis-mediated cartilage degradation. The hormone prolactin (PRL) frequently increases in the circulation of patients with RA, but the role of hyperprolactinemia in disease activity is unclear. Here, we demonstrate that PRL inhibits the apoptosis of cultured chondrocytes in response to a mixture of proinflammatory cytokines (TNF-α, IL-1β, and IFN-γ) by preventing the induction of p53 and decreasing the BAX/BCL-2 ratio through a NO-independent, JAK2/STAT3-dependent pathway. Local treatment with PRL or increasing PRL circulating levels also prevented chondrocyte apoptosis evoked by injecting cytokines into the knee joints of rats, whereas the proapoptotic effect of cytokines was enhanced in PRL receptor-null (Prlr -/-) mice. Moreover, eliciting hyperprolactinemia in rats before or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, proinflammatory cytokine expression, pannus formation, bone erosion, joint swelling, and pain. These results reveal the protective effect of PRL against inflammation-induced chondrocyte apoptosis and the therapeutic potential of hyperprolactinemia to reduce permanent joint damage and inflammation in RA.

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Section: Introductionmentioning

confidence: 99%

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

et al. 2013

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“…Coss and co-workers (2000) also showed that PRLR was widely expressed in the growth plate chondrocytes in the digits of neonatal rats. Besides the growth plate chondrocytes, PRLR expression has been reported in articular chondrocytes from both humans and rats (Ogueta et al 2002;Zermeño et al 2006). In the articular chondrocytes in vitro, PRL has been found to inhibit apoptosis induced by serum starvation (Zermeño et al 2006) and to increase type II collagen expression (Ogueta et al 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Besides the growth plate chondrocytes, PRLR expression has been reported in articular chondrocytes from both humans and rats (Ogueta et al 2002;Zermeño et al 2006). In the articular chondrocytes in vitro, PRL has been found to inhibit apoptosis induced by serum starvation (Zermeño et al 2006) and to increase type II collagen expression (Ogueta et al 2002). Moreover, PRL could directly induce proliferation and chondrogenic differentiation of the human marrow-derived mesenchymal stem cells to mature chondrocytes (Ogueta et al 2002).…”

Section: Discussionmentioning

confidence: 99%

“…After binding to PRL receptors (PRLR) on osteoblasts, PRL induced trabecular bone resorption and calcium release through the synthesis of an osteoblast-derived osteoclastogenic factor, namely receptor activator of nuclear factor-jB ligand (Seriwatanachai et al 2008). Besides the osteoblasts, chondrocytes isolated from the rat articular cartilage were also found to express functional PRLR, which could prevent apoptosis of this cell type in vitro (Zermeño et al 2006). Nevertheless, whether the growth plate changes during pregnancy and lactation were also PRL-dependent remained unknown.…”

Section: Introductionmentioning

confidence: 99%

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Possible chondroregulatory role of prolactin on the tibial growth plate of lactating rats

Suntornsaratoon

Wongdee

Krishnamra

et al. 2010

Histochem Cell Biol

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Besides calcium accretion in the cortical envelope, a marked increase in the length of long bone was observed in pregnant and lactating rats, and thus the growth plate change was anticipated. Since several bone changes, such as massive trabecular bone resorption in late lactation, were found to be prolactin (PRL)-dependent, PRL may also be responsible for the maternal bone elongation. Herein, we investigated the growth plate change and possible chondroregulatory roles of PRL in the tibiae of rats at mid-pregnancy until 15 days postweaning. We found that the tibial length of lactating rats was increased and was inversely correlated with the total growth plate height, as well as the heights of proliferating zone (PZ) and hypertrophic zone (HZ), but not the resting zone (RZ). Chondrocytes in all zones expressed PRL receptors as visualized by immunohistochemistry, suggesting that the growth plate cartilage was a target of PRL action. Further investigations in lactating rats treated with an inhibitor of pituitary PRL release, bromocriptine, with or without PRL supplement, revealed the PRL-induced decreases in total growth plate height and HZ height from early to late lactation. However, decreases in RZ and PZ heights were observed only in late and mid-lactation, respectively. Thus, this was the first report on the chondroregulatory action of PRL on the growth plate of long bone in lactating rats. The results provided better understanding of the maternal bone adaptation during lactation.

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“…Assuming D5 has dopamine agonist properties, this could have detrimental consequences in various immunological diseases, injuries and cancers. • Prolactin has been reported to affect a variety of other cells including human adipocytes (Asai-Sato et al, 2006;Nilsson et al, 2005), mouse adipocytes (Flint et al, 2006) rat cholangiocytes (Bogorad et al, 2006a, b), rat chondrocytes (Zermeno et al, 2006), human natural killer (NK) cells (Sun et al, 2004), developing human thymocytes (Carreno et al, 2005), and rat pancreatic islet cells (Amaral et al, 2004).…”

Section: Other Human Health Concernsmentioning

confidence: 99%

Distribution, Elimination, and Rearrangement of Cyclic Volatile Methylsiloxanes in Oil-Contaminated Soil of the Shengli Oilfield, China

Shi

et al. 2015

Environ. Sci. Technol.

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SUBJECT: REVIEW OF TOXICITY INFORMATION ON D5 ______________________________________________________________________________We are forwarding our review of available information on the toxicity and persistence of decamethylcyclopentasiloxane (D5), a proposed alternative for perchloroethylene in dry cleaning. The review was conducted to provide ARB with information on which to base a determination of whether D5 could be considered a non-toxic alternative to perchloroethylene for dry cleaning under AB 998 (Lowenthal, Chapter 821, Statutes of 2003), pursuant to contract number 05-414. In response to your request to evaluate available information on the toxicity of D5 under the statutory mandate, OEHHA staff have reviewed information submitted by the Silicones Environmental Health and Safety Council (SEHSC), including studies evaluating acute and subchronic toxicity, neuroendocrine activity, estrogenicity, genotoxicity, chronic toxicity and carcinogenicity and related mode of action studies, and pharmacokinetics. In addition, we evaluated an SEHSC white paper summarizing the toxicity of D5, and an exposure assessment conducted by Environ Corporation for SEHSC. We also searched the open literature for additional information, including government documents from other countries, and identified additional information on human exposure, environmental persistence and accumulation in biota. As requested by ARB, we focused on evaluating the applicability of the SEHSC-proposed mechanism of action of tumor formation in rodents to human health risk assessment. Our review of the available information is attached.In the process of reviewing the information, we met three times with the SEHSC representatives, including their toxicologists. We sought outside expertise from the University of California, Davis, regarding the merits of the proposed mode of action of D5 induced tumors in rodents. We also spoke with U.S.EPA scientists, who reviewed materials on D5 toxicity under

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Prolactin inhibits the apoptosis of chondrocytes induced by serum starvation

Cited by 24 publications

References 40 publications

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

Possible chondroregulatory role of prolactin on the tibial growth plate of lactating rats

Distribution, Elimination, and Rearrangement of Cyclic Volatile Methylsiloxanes in Oil-Contaminated Soil of the Shengli Oilfield, China

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