MicroRNA Signature, Regulatory Functions in Endometrium-Normal and Disease
MicroRNA Signature, Regulatory Functions in Endometrium-Normal and Disease
During the menstrual cycle, human endometrium undergoes extensive cyclic morphologic and biochemical modifications in preparation for embryo implantation. These processes are highly regulated by ovarian steroids and various locally expressed gene products and involve inflammatory reaction, apoptosis, cell proliferation, angiogenesis, differentiation (tissue formation), and tissue remodeling. MicroRNAs (miRNAs) have emerged as key regulators of gene expression, and their altered and/or aberrant expression has been associated with establishment and progression of various disorders, including tumorigenesis. This review highlights the endometrial expression of miRNAs and their potential regulatory functions under normal and pathologic conditions such as endometriosis, dysfunctional uterine bleeding, and endometrial cancer. Given the key regulatory function of miRNAs on gene expression stability, understanding the underlying mechanisms of how endometrial miRNAs are regulated and identifying their specific target genes and their functions might lead to the development of preventive and therapeutic strategies by regulating specific target genes associated with such reproductive disorders.
During the menstrual cycle, endometrium undergoes extensive cyclic morphologic and biochemical modifications in preparation for embryo implantation that are remarkably consistent during each cycle throughout the reproductive years. This process, which begins with degenerative signals resulting in menstrual bleeding and endometrial shedding, integrates many overlapping and dynamic events to regenerate and become receptive. The endometrial regenerative process is initiated by an inflammatory reaction followed by a rapid cell proliferation, angiogenesis, differentiation (tissue formation), and tissue remodeling. If conception is not established, endometrium is ready to begin the next cycle. Ovarian sex steroids are central to endometrial regenerative and receptive processes. Accumulative evidence also suggests that endometrial expression of various autocrine/paracrine regulators, including many growth factors, cytokines, chemokines, proteases, and extracellular matrix, serve as key components of these processes. The endometrial expression of these molecules must be optimal, precise, and synchronized to generate a timely progression of their signaling pathways. Any alterations in the expression of these mediators seem to be responsible for inappropriate tissue regeneration, embryo implantation failure, and other uterine abnormalities, including dysfunctional uterine bleeding, endometriosis, and endometrial cancer.
During the menstrual cycle, human endometrium undergoes extensive cyclic morphologic and biochemical modifications in preparation for embryo implantation. These processes are highly regulated by ovarian steroids and various locally expressed gene products and involve inflammatory reaction, apoptosis, cell proliferation, angiogenesis, differentiation (tissue formation), and tissue remodeling. MicroRNAs (miRNAs) have emerged as key regulators of gene expression, and their altered and/or aberrant expression has been associated with establishment and progression of various disorders, including tumorigenesis. This review highlights the endometrial expression of miRNAs and their potential regulatory functions under normal and pathologic conditions such as endometriosis, dysfunctional uterine bleeding, and endometrial cancer. Given the key regulatory function of miRNAs on gene expression stability, understanding the underlying mechanisms of how endometrial miRNAs are regulated and identifying their specific target genes and their functions might lead to the development of preventive and therapeutic strategies by regulating specific target genes associated with such reproductive disorders.
During the menstrual cycle, endometrium undergoes extensive cyclic morphologic and biochemical modifications in preparation for embryo implantation that are remarkably consistent during each cycle throughout the reproductive years. This process, which begins with degenerative signals resulting in menstrual bleeding and endometrial shedding, integrates many overlapping and dynamic events to regenerate and become receptive. The endometrial regenerative process is initiated by an inflammatory reaction followed by a rapid cell proliferation, angiogenesis, differentiation (tissue formation), and tissue remodeling. If conception is not established, endometrium is ready to begin the next cycle. Ovarian sex steroids are central to endometrial regenerative and receptive processes. Accumulative evidence also suggests that endometrial expression of various autocrine/paracrine regulators, including many growth factors, cytokines, chemokines, proteases, and extracellular matrix, serve as key components of these processes. The endometrial expression of these molecules must be optimal, precise, and synchronized to generate a timely progression of their signaling pathways. Any alterations in the expression of these mediators seem to be responsible for inappropriate tissue regeneration, embryo implantation failure, and other uterine abnormalities, including dysfunctional uterine bleeding, endometriosis, and endometrial cancer.
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