Potential role ofHOXD9 in synoviocyte proliferation

Khoa, Nguyen Dinh; Nakazawa, Minako; Hasunuma, Tomoko; Nakajima, Takeshi; Nakamura, Hiroshi; Kobata, Tetsuji; Nishioka, Kusuki

doi:10.1002/1529-0131(200105)44:5<1013::aid-anr180>3.0.co;2-o

Cited by 10 publications

(1 citation statement)

References 40 publications

(53 reference statements)

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“…We re-clustered the mesenchymal and stromal cells (Figure 4A) yielding 21 new clusters to pursue a higher resolution picture of thecal expansion (Figure 4A'; Figure S5D). The re-clustered mesenchymal cells fell into eight groups, STCs expressing Cyp17a1, Tagln-expressing fibroblasts (Sun et al, 2023), Col14a1-expressing fibroblasts (Xie et al, 2018), Cd24a-expressing fibroblasts (Wang et al, 2022), Cxcl14-expressing fibroblasts (Sjoberg et al, 2019), Hox9-expressing fibroblasts (Khoa et al, 2001, and mitotic cells expressing Mki67 (Figure 4C, C').…”

Section: Analysis Of Selected Mesenchymal Cellsmentioning

confidence: 99%

Three waves of ovarian follicles in juvenile mice

Yin,

Spradling

2024

Preprint

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The earliest mouse fetal ovarian follicles (wave 1) grow rapidly in the ovarian medulla but their function remains unclear. We found these follicles do not produce mature oocytes but follow a distinct developmental program. At preantral stages, their oocytes and then most granulosa cells turn over. Thecal cells expand further, vascularize, express androgen biosynthetic genes, consistent with scRNAseq analyses. In contrast, normal follicles begin to arise during week two from primordial follicles near the medullar-cortical boundary with mosaic granulosa cells. The highest levels of androgen biosynthetic gene expression occur in the thecal network at 5 weeks, a period known as “peri-puberty,” and may influence sexually dimorphic brain development and reproductive behavior. Abnormalities of thecal network formation or function in humans may contribute to polycystic ovarian syndrome.

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Section: Analysis Of Selected Mesenchymal Cellsmentioning

confidence: 99%

Three waves of ovarian follicles in juvenile mice

Yin,

Spradling

2024

Preprint

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Induction of RANKL expression and osteoclast maturation by the binding of fibroblast growth factor 2 to heparan sulfate proteoglycan on rheumatoid synovial fibroblasts

Nakano¹,

Okada²,

Saito³

et al. 2004

Arthritis & Rheumatism

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Objective. Rheumatoid arthritis (RA) is characterized by progressive joint destruction. The aim of this study was to clarify the relevance of RA synovial fibroblasts (RASFs) and fibroblast growth factor 2 (FGF-2), which is produced abundantly by RASFs, to the osteoclastogenesis and bone resorption in RA.Methods. Synovial fibroblasts were prepared from the synovial tissues of 10 patients with active RA and 7 patients with osteoarthritis (OA). The expression of RANKL, intercellular adhesion molecule 1 (ICAM-1), FGF receptor 1 (FGFR-1), and heparan sulfate proteoglycan (HSPG) on synovial fibroblasts was measured by FACScan. Osteoclast formation in cocultures of RASFs and peripheral blood mononuclear cells (PBMCs) was evaluated by tartrate-resistant acid phosphatase staining and a pit-formation assay using dentin slices.Results. FGF-2 induced the expression of both RANKL and ICAM-1 on RASFs more so than on OA synovial fibroblasts (OASFs). FGF-2-induced upregulation of RANKL and ICAM-1 was inhibited by anti-FGF-2 antibody. Although FGFR-1 was equally expressed on RASFs and OASFs, HSPG was highly expressed on RASFs. Up-regulation of RANKL by FGF-2 on RASFs was diminished by the removal of heparan sulfate with heparitinase. Osteoclast formation from PBMCs induced by RASFs was inhibited by the addition of either heparitinase, anti-ICAM-1 antibody, anti-FGF-2 antibody, or osteoprotegerin. FGF-2-induced RANKL on RASFs and osteoclast formation were suppressed by an inhibitor of ERK.Conclusion. FGF-2 was transferred to FGFR-1 through binding to HSPG, which is characteristically expressed on RASFs, resulting in RANKL-and ICAM-1-mediated maturation of osteoclasts via ERK activation. Thus, we propose that FGF-2 not only augments the proliferation of RASFs, but also is involved in osteoclast maturation, which leads to bone destruction in RA.

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