Role of Apoptosis in Normal and Abnormal Development

2008 ◽  
pp. 13-54
Keyword(s):  
Abnormal Development

scholarly journals MiR-125 Family in Cardiovascular and Cerebrovascular Diseases

2021 ◽  
Vol 9 ◽  
Author(s):  
Yang Wang ◽  
Jing Tan ◽  
Lu Wang ◽  
Gaiqin Pei ◽  
Hongxin Cheng ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Ischemia Reperfusion Injury ◽  
Mirna Family ◽  
Ischemia Reperfusion ◽  
Cerebrovascular Diseases ◽  
Clinical Applications ◽  
Abnormal Development ◽  
Prevention And Treatment ◽  
Huge Challenge

Cardiovascular and cerebrovascular diseases are a serious threaten to the health of modern people. Understanding the mechanism of occurrence and development of cardiovascular and cerebrovascular diseases, as well as reasonable prevention and treatment of them, is a huge challenge that we are currently facing. The miR-125 family consists of hsa-miR-125a, hsa-miR-125b-1 and hsa-miR-125b-2. It is a kind of miRNA family that is highly conserved among different species. A large amount of literature shows that the lack of miR-125 can cause abnormal development of the cardiovascular system in the embryonic period. At the same time, the miR-125 family participates in the occurrence and development of a variety of cardiovascular and cerebrovascular diseases, including myocardial ischemia, atherosclerosis, ischemia-reperfusion injury, ischemic stroke, and heart failure directly or indirectly. In this article, we summarized the role of the miR-125 family in the development and maturation of cardiovascular system, the occurrence and development of cardiovascular and cerebrovascular diseases, and its important value in the current fiery stem cell therapy. In addition, we presented this in the form of table and diagrams. We also discussed the difficulties and challenges faced by the miR-125 family in clinical applications.

scholarly journals Suppression of Insulin-Like3 Receptor Reveals the Role of β-Catenin and Notch Signaling in Gubernaculum Development

2011 ◽  
Vol 25 (1) ◽  
pp. 170-183 ◽  
Author(s):  
Elena M. Kaftanovskaya ◽  
Shu Feng ◽  
Zaohua Huang ◽  
Yingchun Tan ◽  
Agustin M. Barbara ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myogenic Differentiation ◽  
Critical Role ◽  
Abnormal Development ◽  
Testicular Descent ◽  
Hypomorphic Allele ◽  
Conditional Suppression ◽  
Notch Pathways ◽  
Cellular Components

During male development, the testes move from a high intraabdominal position and descend into the scrotum. The gubernaculum, an inguinoscrotal ligament connecting the testis to the lower abdomen, is believed to play a critical role in this process. The first stage of testicular descent is controlled by insulin like3 hormone (INSL3), produced in testicular Leydig cells. Deletion of Insl3 or its receptor, Rxfp2, in mice causes cryptorchidism. We produced Cre/loxP regulated shRNA transgenic mice targeting RXFP2 expression. We have shown that the transgene was able to reduce Rxfp2 gene expression and thus behaved as a hypomorphic allele of Rxfp2. Variable degrees of uni- and bilateral cryptorchidism was detected in males with the activated shRNA transgene on an Rxfp2+/− background. Conditional suppression of Rxfp2 in the gubernaculum led to cryptorchidism. Gene expression analysis of a mutant cremasteric sac using Illumina microarrays indicated abnormal expression of a significant number of genes in Wnt/β-catenin and Notch pathways. We have demonstrated profound changes in the expression pattern of β-catenin, Notch1, desmin, and androgen receptor (AR), in Rxfp2−/− male embryos, indicating the role of INSL3 in proliferation, differentiation, and survival of specific cellular components of the gubernaculum. We have shown that INSL3/RXFP2 signaling is essential for myogenic differentiation and maintenance of AR-positive cells in the gubernaculum. Males with the deletion of β-catenin or Notch1 in the gubernacular ligament demonstrated abnormal development. Our data indicates that β-catenin and Notch pathways are potential targets of INSL3 signaling during gubernacular development.

scholarly journals What it is said versus how it is said: Comprehension of affective prosody in men with Klinefelter (47,XXY) syndrome

2007 ◽  
Vol 13 (6) ◽  
pp. 1065-1070 ◽  
Author(s):  
SOPHIE VAN RIJN ◽  
ANDRÉ ALEMAN ◽  
HANNA SWAAB ◽  
TESSEL KRIJN ◽  
GUY VINGERHOETS ◽  
...  
Keyword(s):  
Social Communication ◽  
Right Hemisphere ◽  
Klinefelter Syndrome ◽  
Abnormal Development ◽  
Affective Prosody ◽  
Language Functions ◽  
Verbal Content ◽  
Pragmatic Aspect ◽  
Tone Of Voice

Difficulties in social communication in individuals with Klinefelter syndrome (XXY chromosomal pattern) have largely been attributed to deficits in left hemisphere-mediated, language functions. This study examined the ability of XXY men to decode emotions from tone of voice, a pragmatic aspect of social communication that may be associated with right hemisphere functioning. A total of 26 XXY men and 20 men from the general population completed tasks involving emotion discrimination in speech, based on verbal content or tone of voice. The XXY group displayed relative difficulties in discriminating emotions in tone of voice, and, to a lesser extend, in verbal content. This finding suggests that the XXY chromosomal pattern may not only be associated with difficulties in semantic aspects of language, but with prosodic aspects, as well. Our findings may contribute to the development of more comprehensive models addressing the role of the X chromosome in normal and abnormal development of social communication. (JINS, 2007, 13, 1065–1070.)

scholarly journals Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder

2020 ◽  
Vol 10 (12) ◽  
pp. 951
Author(s):  
Alma Y. Galvez-Contreras ◽  
David Zarate-Lopez ◽  
Ana L. Torres-Chavez ◽  
Oscar Gonzalez-Perez
Keyword(s):  
Autism Spectrum Disorder ◽  
Interpersonal Communication ◽  
Neurodevelopmental Disorder ◽  
Brain Regions ◽  
Autism Spectrum ◽  
Repetitive Behaviors ◽  
Spectrum Disorder ◽  
Abnormal Development ◽  
Matter Production

Autism Spectrum Disorder (ASD) is an early neurodevelopmental disorder that involves deficits in interpersonal communication, social interaction, and repetitive behaviors. Although ASD pathophysiology is still uncertain, alterations in the abnormal development of the frontal lobe, limbic areas, and putamen generate an imbalance between inhibition and excitation of neuronal activity. Interestingly, recent findings suggest that a disruption in neuronal connectivity is associated with neural alterations in white matter production and myelination in diverse brain regions of patients with ASD. This review is aimed to summarize the most recent evidence that supports the notion that abnormalities in the oligodendrocyte generation and axonal myelination in specific brain regions are involved in the pathophysiology of ASD. Fundamental molecular mediators of these pathological processes are also examined. Determining the role of alterations in oligodendrogenesis and myelination is a fundamental step to understand the pathophysiology of ASD and identify possible therapeutic targets.

scholarly journals CRISPR-Cas9-mediated mutagenesis of the SlSRM1-like gene leads to abnormal leaf development in tomatoes

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Yao Tang ◽  
Huijia Li ◽  
Chunxin Liu ◽  
Yuqing He ◽  
Hexuan Wang ◽  
...  
Keyword(s):  
Leaf Development ◽  
Carbon Sources ◽  
Tomato Leaf ◽  
Abnormal Development ◽  
Functional Study ◽  
Loss Of Function ◽  
Growth Environment ◽  
Hormone Synthesis ◽  
Short Palindromic Repeat

Abstract Background Leaves, which are the most important organs of plants, can not only fix carbon sources through photosynthesis, but also absorb nutrients through transpiration. Leaf development directly determines the growth, flowering and fruiting of plants. There are many factors that affect leaf development, such as the growth environment, gene expression, and hormone synthesis. In this study, tomatoes were used to study the role of the transcription factor Solanum lycopersicum salt-related MYB1-like (SlSRM1-like) in the development of tomato leaves. Results Loss-of-function of the SlSRM1-like gene mediated by clustered, regularly interspaced, short palindromic repeat (CRISPR)/CRISPR-associated 9 (Cas9) resulted in abnormal tomato leaf morphology, including thinner leaves, wrinkled edges, raised veins, disordered edge veins, and left and right asymmetry. An analysis of the transcription levels of genes related to leaf development revealed that the expression of these genes was significantly altered in the SlSRM1-like mutants (SlSRM1-like-Ms). Moreover, the SlSRM1-like gene was expressed at higher transcription levels in young tissues than in old tissues, and its expression was also induced in response to auxin. In addition, the transcription levels of genes related to the auxin pathway, which regulates tomato growth and development, were severely affected in the SlSRM1-like-Ms. Therefore, it is hypothesized that the SlSRM1-like gene functions in the regulation of tomato leaf development through the auxin-related pathway. Conclusions In this study, we successfully knocked out the SlSRM1-like gene in the tomato variety Ailsa Craig using CRISPR technology and found that knockout of the SlSRM1-like gene resulted in abnormal development of tomato leaves. Further research indicated that SlSRM1-like regulated tomato leaf development through auxin-related pathways. The results provide an important reference for the functional study of other SRM1-like genes in plants and provide new insights into the regulation of leaf development in tomato and other plants.

scholarly journals Role of calcium ions in the control of embryogenesis of Xenopus. Changes in the subcellular distribution of calcium in early cleavage embryos after treatment with the ionophore A23187.

1979 ◽  
Vol 80 (3) ◽  
pp. 589-604 ◽  
Author(s):  
J C Osborn ◽  
C J Duncan ◽  
J L Smith
Keyword(s):  
Divalent Cations ◽  
Subsequent Development ◽  
Abnormal Development ◽  
Ionophore A23187 ◽  
Early Cleavage ◽  
Amphibian Embryo ◽  
High Incidence ◽  
Intracellular Action

Treatment of stage 5 Xenopus embryos with the ionophore A23187 for only 10 min, in the absence of extracellular Mg2+ and Ca2+, causes cortical contractions and a high incidence of abnormal embryos during subsequent development. Cation analysis shows that divalent ions are not lost from the embryos, but that Ca2+ is redistributed within the subcellular fractions. Ca2+ is probably released from yolk platelets and/or pigment granules by the action of A23187, [Ca2+] rises in the cytosol, and the mitochondria attempt to take up this free Ca2+. The mitochondria concomitantly undergo characteristic ultrastructural transformations, changing towards energized-twisted and energized-zigzag conformations. A23187 allows these changes to be demonstrated in situ. Extracellular divalent cations (10(-4) M) interfere with this intracellular action of A23187. Intracellular accumulation of Na+ (by treatment with ouabain) or Li+ also causes abnormal development, probably by promoting a release of Ca2+ from the mitochondria. It is suggested (a) that all these treatments cause a rise in [Ca2+]i which interferes with normal, integrated cell division, so causing, in turn, abnormal embryogenesis, (b) that levels of [Ca2+]i are of importance in regulating cleavage, (c) that the mitochondria could well have a function in regulating [Ca2+]i during embryogenesis in Xenopus, and (d) that vegetalizing agents may well act by promoting a rise in [Ca2+]i in specific cells in the amphibian embryo.

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