Expression of Hyaluronan Synthase 1 and Distribution of Hyaluronan During Follicular Atresia in Pig Ovaries1

Miyake, Yuko; Sakurai, Masahiro; Tanaka, Sadao; Tunjung, Woro Anindito Sri; Yokoo, Masaki; Matsumoto, Hiromichi; Aso, Hisashi; Yamaguchi, Takahiro; Sato, Eimei

doi:10.1095/biolreprod.108.067694

Cited by 10 publications

(8 citation statements)

References 47 publications

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“…As has been described above, the expression of each HAS isoform is spatially and temporally controlled (Itano 2008). In the ovaries of mammals, it has been revealed that all HAS isoforms are expressed at mRNA levels by RT-PCR and that HAS1 and HAS2 proteins are mainly localized in the theca and granulosa cell regions of mature antral follicles respectively (Richards 2005, Miyake et al 2009. In this study, by carrying out in situ hybridization, for the first time, we demonstrated that the expression of Has1 and Has2 mRNAs occurs not only in antral follicles but also in small preantral follicles.…”

Section: Discussionmentioning

confidence: 93%

Involvement of hyaluronan synthesis in ovarian follicle growth in rats

Takahashi¹,

Tarumi

Ishizuka

2014

Reproduction

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Most of the previous studies on ovarian hyaluronan (HA) have focused on mature antral follicles or corpora lutea, but scarcely on small preantral follicles. Moreover, the origin of follicular HA is unknown. To clarify the localization of HA and its synthases in small growing follicles, involvement of HA in follicle growth, and gonadotropin regulation of HA synthase (Has) gene expression, in this study, perinatal, immature, and adult ovaries of Wistar-Imamichi rats were examined histologically and biochemically and by in vitro follicle culture. HA was detected in the extracellular matrix of granulosa and theca cell layers of primary follicles and more advanced follicles. Ovarian HA accumulation ontogenetically started in the sex cords of perinatal rats, and its primary site shifted to the intrafollicular region of primary follicles within 5 days of birth. The Has1-3 mRNAs were expressed in the ovaries of perinatal, prepubertal, and adult rats, and the expression levels of Has1 and Has2 genes were modulated during the estrous cycle in adult rats and following administration of exogenous gonadotropins in immature acyclic rats. The Has1 and Has2 mRNAs were predominantly localized in the theca and granulosa cell layers of growing follicles respectively. Treatments with chemicals known to reduce ovarian HA synthesis induced follicular atresia. More directly, the addition of Streptomyces hyaluronidase, which specifically degrades HA, induced the arrest of follicle growth in an in vitro culture system. These results indicate that gonadotropin-regulated HA synthesis is involved in normal follicle growth.

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Section: Discussionmentioning

confidence: 93%

Involvement of hyaluronan synthesis in ovarian follicle growth in rats

Takahashi¹,

Tarumi

Ishizuka

2014

Reproduction

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“…The enzyme responsible for the polymerisation of hyaluronan in the follicle before ovulation is HAS1, at least in pigs. It is expressed at a higher level in the theca of porcine follicles in comparison to granulosa cells, but is upregulated in granulosa cells late in atresia while hyaluronan levels also increased late in atresia (Miyake et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Glycomic analyses of ovarian follicles during development and atresia

et al. 2012

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To examine the detailed composition of glycosaminoglycans during bovine ovarian follicular development and atresia, the specialized stromal theca layers were separated from the stratified epithelial granulosa cells of healthy (n = 6) and atretic (n = 6) follicles in each of three size ranges: small (3–5 mm), medium (6-9 mm) and large (10 mm or more) (n = 29 animals). Fluorophore-assisted carbohydrate electrophoresis analyses (on a per cell basis) and immunohistochemistry (n = 14) were undertaken. We identified the major disaccharides in thecal layers and the membrana granulosa as chondroitin sulfate-derived ∆uronic acid with 4-sulfated N-acetylgalactosamine and ∆uronic acid with 6-sulfated N-acetylgalactosamine and the heparan sulfate-derived Δuronic acid with N-acetlyglucosamine, with elevated levels in the thecal layers. Increasing follicle size and atresia was associated with increased levels of some disaccharides. We concluded that versican contains 4-sulfated N-acetylgalactosamine and it is the predominant 4-sulfated N-acetylgalactosamine proteoglycan in antral follicles. At least one other non- or 6-sulfated N-acetylgalactosamine proteoglycan(s), which is not decorin or an inter-α-trypsin inhibitor family member, is present in bovine antral follicles and associated with hitherto unknown groups of cells around some larger blood vessels. These areas stained positively for chondroitin/dermatan sulfate epitopes [antibodies 7D4, 3C5, and 4C3], similar to stem cell niches observed in other tissues. The sulfation pattern of heparan sulfate glycosaminoglycans appears uniform across follicles of different sizes and in healthy and atretic follicles. The heparan sulfate products detected in the follicles are likely to be associated with perlecan, collagen XVIII or betaglycan.

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“…It is synthetized in granulosa cells and secreted into the follicular fluid where it maintains folliculogenesis and prevents oocyte degeneration (86,98). Hyaluronan degradation may be associated with follicular atresia (71). In all controls analyzed, ranging from 1 month to 45 years of age, hyaluronan was detected in growing preantral cells and mature Graafian follicles and surrounded by granulosa cells expressing the hyaluronan receptor CD44.…”

Section: Extra-cerebral Involvementmentioning

confidence: 99%

Vanishing white matter: a leukodystrophy due to astrocytic dysfunction

et al. 2018

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VWM is one of the most prevalent leukodystrophies with unique clinical, pathological and molecular features. It mostly affects children, but may develop at all ages, from birth to senescence. It is dominated by cerebellar ataxia and susceptible to stresses that act as factors provoking disease onset or episodes of rapid neurological deterioration possibly leading to death. VWM is caused by mutations in any of the genes encoding the five subunits of the eukaryotic translation initiation factor 2B (eIF2B). Although eIF2B is ubiquitously expressed, VWM primarily manifests as a leukodystrophy with increasing white matter rarefaction and cystic degeneration, meager astrogliosis with no glial scarring and dysmorphic immature astrocytes and increased numbers of oligodendrocyte progenitor cells that are restrained from maturing into myelin-forming cells. Recent findings point to a central role for astrocytes in driving the brain pathology, with secondary effects on both oligodendroglia and axons. In this, VWM belongs to the growing group of astrocytopathies, in which loss of essential astrocytic functions and gain of detrimental functions drive degeneration of the white matter. Additional disease mechanisms include activation of the unfolded protein response with constitutive predisposition to cellular stress, failure of astrocyte-microglia crosstalk and possibly secondary effects on the oxidative phosphorylation. VWM involves a translation initiation factor. The group of leukodystrophies due to defects in mRNA translation is also growing, suggesting that this may be a common disease mechanism. The combination of all these features makes VWM an intriguing natural model to understand the biology and pathology of the white matter.

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Expression of Hyaluronan Synthase 1 and Distribution of Hyaluronan During Follicular Atresia in Pig Ovaries1

Cited by 10 publications

References 47 publications

Involvement of hyaluronan synthesis in ovarian follicle growth in rats

Involvement of hyaluronan synthesis in ovarian follicle growth in rats

Glycomic analyses of ovarian follicles during development and atresia

Vanishing white matter: a leukodystrophy due to astrocytic dysfunction

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