<p>Telocytes are specialized stromal cells involved in intercellular signaling and tissue homeostasis. Despite studies on their association with various diseases of female reproductive organs, their contribution to early pregnancy loss is poorly understood. This study aimed to investigate alterations in stromal cell populations exhibiting immunophenotypic overlap with telocytes in first-trimester spontaneous abortion and to evaluate their potential role in stromal dysregulation. Endometrial tissues from first-trimester spontaneous abortus (<i>n</i> = 70) and non-pregnant endometrial curettage cases as control (<i>n</i> = 70) were retrospectively analyzed. Cases with neoplastic diagnoses including endometrial hyperplasia, endometrial carcinoma, endometrial stromal tumors, leiomyoma, and leiomyosarcoma, were excluded. Immunohistochemical staining for CD34, CD117, and PDGFR-α was performed, quantitative immunoreactivity analysis was conducted using ImageJ program and statistically analyzed. CD34 immunoreactivity was observed in vascular endothelium and stromal cells, with comparable vascular density and stromal distribution between groups. CD117-positive stromal cells, mainly observed in endometrial stroma, were reduced in abortus tissues (<i>p</i> = 0.022). PDGFR-α expression was seen in stromal cell bodies and showed marked decrease in abortus group compared to control (<i>p</i> &lt; 0.001). No significant staining was observed in luminal or glandular epithelium for CD117 and PDGFR-α. First-trimester pregnancy loss is associated with impairment of putative telocyte related stromal marker expressions, particularly PDGFR-α, while CD117 reduction was observed and vascular parameters remain preserved. These findings suggest that disruption of stromal cellular communication and microenvironmental regulation, rather than vascular deficiency, might contribute to early pregnancy loss. Further studies incorporating ultrastructural and various molecular approaches are needed to clarify the functional and clinical significance and involvement of telocytes in pregnancy loss.</p>

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Immunohistochemical Alterations of Putative Telocyte-Associated Stromal Markers in Early Pregnancy Loss: A Retrospective Study

  • Dila Sener-Akcora,
  • Alp Eren Ornek,
  • Ugur Seker,
  • Yasemin Ersoy Canıllıoglu,
  • Ozlem Yapıcıer

摘要

Telocytes are specialized stromal cells involved in intercellular signaling and tissue homeostasis. Despite studies on their association with various diseases of female reproductive organs, their contribution to early pregnancy loss is poorly understood. This study aimed to investigate alterations in stromal cell populations exhibiting immunophenotypic overlap with telocytes in first-trimester spontaneous abortion and to evaluate their potential role in stromal dysregulation. Endometrial tissues from first-trimester spontaneous abortus (n = 70) and non-pregnant endometrial curettage cases as control (n = 70) were retrospectively analyzed. Cases with neoplastic diagnoses including endometrial hyperplasia, endometrial carcinoma, endometrial stromal tumors, leiomyoma, and leiomyosarcoma, were excluded. Immunohistochemical staining for CD34, CD117, and PDGFR-α was performed, quantitative immunoreactivity analysis was conducted using ImageJ program and statistically analyzed. CD34 immunoreactivity was observed in vascular endothelium and stromal cells, with comparable vascular density and stromal distribution between groups. CD117-positive stromal cells, mainly observed in endometrial stroma, were reduced in abortus tissues (p = 0.022). PDGFR-α expression was seen in stromal cell bodies and showed marked decrease in abortus group compared to control (p < 0.001). No significant staining was observed in luminal or glandular epithelium for CD117 and PDGFR-α. First-trimester pregnancy loss is associated with impairment of putative telocyte related stromal marker expressions, particularly PDGFR-α, while CD117 reduction was observed and vascular parameters remain preserved. These findings suggest that disruption of stromal cellular communication and microenvironmental regulation, rather than vascular deficiency, might contribute to early pregnancy loss. Further studies incorporating ultrastructural and various molecular approaches are needed to clarify the functional and clinical significance and involvement of telocytes in pregnancy loss.