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Mother and Embryo Cross Communication during Conception
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Anna Idelevich, Andrea Peralta, Felipe Vilella
Homeobox protein A10, A11 (HOXA10, HOXA11) play a role in decidualization, and their deletion in mice results in implantation defects [122,123]. HOXA10-null mice produce normal numbers of embryos that are able to implant in wild-type surrogate mice, whereas wild-type embryos from the surrogate mice cannot implant in the HOXA10-null mice [122,124]. HOXA11−/− mice show similar phenotype related to implantation [125]. In the human endometrium, HOXA10 is expressed by both epithelial and stromal cells in a menstrual cycle-dependent manner and is regulated by progesterone [126]. Microarray analysis of murine endometrium transfected with HOXA10 cDNA identified 40 downstream target genes including clusterin (Clu), phosphoglycerate 3-dehydrogenase (3-Pgdh), and tumor-associated calcium signal transducer 2 (Tacstd2) [127].
Breach of the Endometrial Cavity during Myomectomy and Its Implications for Subsequent Fertility
Published in Rooma Sinha, Arnold P. Advincula, Kurian Joseph, FIBROID UTERUS Surgical Challenges in Minimal Access Surgery, 2020
Increased uterine contractility, disturbances in endometrial cytokine expression, abnormal vascularization, and chronic endometrial inflammation are mechanisms that harm embryo implantation [3]. Another mechanism that has undergone evaluation is the reduction of HOXA-10 levels in the endometrium [4].
Leiomyomata and Reproduction
Published in John C. Petrozza, Uterine Fibroids, 2020
Leiomyomata are responsive to sex steroids and secrete and respond to inflammatory and vasoactive factors. Aberrant excessive production of transforming growth factor-beta (TGF-β), a multifunctional cytokine, from fibroids has been reported by several investigators [10,11] and has been implicated in altered implantation of the embryo [12]. Homeobox A10 (HOXA-10) is one of the most recognized gene sequences in mammalian implantation. Lower levels of expression have been identified in endometrial specimens in patients with fibroids [13,14]. Altered growth-factor secretion may lead to abnormal vasculature, characterized by dilated venous plexuses and disordered angiogenesis [15,16].
Zooming in on the endometrial factor of recurrent implantation failure
Published in Human Fertility, 2022
Chibuzor Ifenatuoha, Babatunde Okewale
The Müllerian ducts are paired structures formed during embryonic development that give rise to the uterus, Fallopian tubes, uterine cervix, and the anterior part of the vagina (Robboy et al., 2017). Typically, the formation of the Müllerian duct takes in three phases, which are: (i) organogenesis (when the ducts are formed); (ii) fusion (when the ducts fuse to form the uterus); and (iii) septal resorption (when the central septum is finally resorbed after the fusion of the ducts). Any anomaly that would result in the failure of completion of the organogenesis phase may result in uterine agenesis, hypoplasia, or a unicornuate uterus. Similarly, the failure in completion of the fusion and septal resorption phases will result in a bicornuate or didephys uterus and a septate or arcuate uterus respectively (Chandler et al., 2009). It was estimated that about 3.8 to 9.6% of the general population have abnormal uterine formation (Santamaria et al., 2018). Mutation in the homeobox genes (HOXA10 and HOXA11) are said to be responsible for Mullerian duct malformation. The homeobox gene family is commonly responsible for the regulation of the Müllerian duct formation. In addition, the HOXA10 and HOXA11 are said to also play a role in endometrial development and preparing the endometrium for implantation (Coughlan et al., 2014).
Homeobox A5 and A9 expression and beta-thalassemia
Published in British Journal of Biomedical Science, 2021
EAE Badr, IE-T El-Sayed, MKR Alasadi
Data from zebrafish point to Homeobox (Hox) genes having an important role in normal haematopoiesis related to haematopoietic stem cells (HSCs) and early haematopoietic progenitors [6]. The Hox genes contain several clusters (A-D). Each cluster consists of paralog groups with nine to eleven members assigned on the basis of sequence similarity and relative position within the cluster [7]. The HOXA family encodes proteins that contain the DNA-binding homeobox motif and controls the early patterns of embryo segmentation. Although HOX expression is typically inhibited in adults, reactivation may occur with various homoeostatic cellular processes including haematopoiesis. Hox genes are required for the maintenance of progenitor or stem cell status, promoting their proliferation. HoxA9 is the most preferentially expressed Hox gene in human CD34+ HSCs and early haematopoietic progenitors [8]. HoxA5 has two effects on erythropoiesis: it causes a predominance of mature erythroid lineage cells and the partial apoptosis of erythroid progenitors. RNA-seq indicates that multiple biological processes including erythrocyte homoeostasis, cell metabolism, and apoptosis are modified by HoxA5 [9]. We hypothesized roles for HoxA9 and HoxA5 in β-thalassemia.
Progestogens and pregnancy loss
Published in Climacteric, 2018
In the menstrual cycle, progesterone is secreted by the corpus luteum and converts the proliferative endometrium into a secretory endometrium, which is characterized by inhibition of the endometrial proliferation induced by estrogen. Under the influence of progesterone, the endometrial glands and blood vessels become more tortuous. Glycogen accumulates in the vacuoles of the glandular cells, leading to secretion of glycoproteins and peptides into the endometrial cavity. The stroma becomes edematous, and progesterone leads to stromal cell transformation into decidual cells, with accompanying infiltration of natural killer (NK) cells, T cells, and macrophages. Pinopode formation coincides with increased progesterone levels during the window of implantation1. Pinopodes may extract fluid from the uterus, facilitating closer contact between blastocyst and endometrium2. Progesterone increases osteopontin (a ligand for integrin αvβ3 secretion), a bridging molecule between the embryo and endometrium. In the mid-luteal phase, leukemia inhibitory factor (LIF, a cytokine essential for implantation in muridae) is upregulated. In fact, antiprogestin treatment results in reduced LIF expression. HOXA-10 and -11 genes are up-regulated by estrogen and progesterone. HOXA-10 mediates integrin involvement in early embryo–endometrial interactions and HOXA-10 expression is required for pinopode formation in the mouse.