IGF-I slightly improves nuclear maturation and cleavage rate of bovine oocytes exposed to acute heat shock<i>in vitro</i>

Qi, Mei-Yu; Liu, Di; Roth, Zvi

doi:10.1017/s096719941400015x

Cited by 21 publications

(15 citation statements)

References 51 publications

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“…In a study conducted by Zhandi et al [33], addition of 100 ng/mL IGF1 during IVM enhanced heat shock-induced apoptosis and compromised developmental competence of heatshocked oocytes. In contrast, Meiyu et al [34] found that addition of 100 ng/mL IGF1 during IVM prevented heat shock-induced apoptosis in bovine oocytes. Therefore, the objective of this study was to determine the role of IGF1 on nuclear maturation, apoptosis, mitochondrial activity, cytoskeleton organization, and developmental competence of bovine oocytes exposed to heat shock during IVM.…”

Section: Introductionmentioning

confidence: 85%

Thermoprotective effect of insulin-like growth factor 1 on in vitro matured bovine oocyte exposed to heat shock

et al. 2016

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a b s t r a c tThe role of insulin-like growth factor 1 (IGF1) on cellular function and developmental capacity of heat-shocked oocytes has not been completely understood. Therefore, the objective of this study was to determine the effect of IGF1 on apoptosis, mitochondrial activity, cytoskeletal changes, nuclear maturation, and developmental competence of bovine oocytes exposed to heat shock. Cumulus-oocyte complexes were submitted to control (38.5 C for 22 hours) and heat shock (41 C for 14 hours followed by 38.5 C for 8 hours) in the presence of 0 or 100 ng/mL IGF1 during IVM. Heat shock increased the percentage of TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling)-positive oocyte and reduced oocyte mitochondrial activity. However, addition of 100 ng/mL IGF1 minimized these deleterious effects of temperature. Caspase activity was affected neither by heat shock nor IGF1. Exposure of bovine oocytes to 41 C during the first 14-hour IVM affected cortical actin localization and microtubule organization at the meiotic spindle and reduced the percentage oocytes that reached the metaphase II stage. However, in the presence of IGF1, cortical actin and percentage of metaphase II oocytes were not different between control and heat-shocked oocytes, suggesting a partial beneficial effect of IGF1. There was no effect of IGF1 on microtubule organization. Heat shock also reduced the percentage of oocytes that reached the blastocyst stage, blastocyst cell number, and increased the percentage of TUNELpositive blastomeres. However, there was no effect of 100 ng/mL IGF1 on oocyte development to the blastocyst stage and blastocyst quality. Therefore, 100 ng/mL IGF1 prevented some heat shock-induced cellular damage in bovine oocytes but had no effect on oocyte developmental competence. In contrast, a low IGF1 concentration (25 ng/mL) had a thermoprotective effect on oocyte developmental competence to the blastocyst stage. In conclusion, IGF1 prevented part of the damage induced by heat shock on oocyte function. This effect was modulated by IGF1 concentration.

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Section: Introductionmentioning

confidence: 85%

Thermoprotective effect of insulin-like growth factor 1 on in vitro matured bovine oocyte exposed to heat shock

et al. 2016

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“…The detrimental effect of heat shock during IVM on cleavage rate of IVF embryos is contradictory, being supported by some studies (Kalo & Roth, ; Roth & Hansen, , ), but not by others (Edwards et al, ; Edwards, Saxton, Lawrence, Payton, & Dunlap, ; Ju, Jiang, Tseng, Parks, & Yang, ). Nevertheless, it was reported that a lower percentage of oocytes developed towards 4‐cell stage at 44 hr post‐insemination when IVM was performed under heat shock conditions, suggesting that the high temperature during oocyte maturation can impair the second embryonic division (Meiyu, Liu, & Roth, ). Other study reported lower proportion of embryos with 3–4 cells at 70–72 hr post‐fertilization when in vitro maturation was performed under 40°C (Diez et al, ).…”

Section: Discussionmentioning

confidence: 99%

Contrasting effects of heat shock during in vitro maturation on development of in vitro‐fertilized and parthenogenetic bovine embryos

Camargo

Costa

Munk

et al. 2019

Reprod Domestic Animals

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This study investigated the influence of heat shock during in vitro maturation on embryo development following in vitro fertilization (IVF) or parthenogenesis (Part). Immature bovine cumulus–oocyte complexes were exposed to heat shock (41.0°C) during the first 12 hr of in vitro maturation (IVM), followed by 12 hr at 38.5°C. Control group consisted of in vitro maturation for 24 hr at 38.5°C. Oocytes were in vitro‐fertilized or activated with ionomycin and cultured in vitro for 192 hr post‐in vitro insemination or parthenogenetic activation (hpia). There was an interaction (p < .01) between temperature of IVM and method of oocyte activation (IVF or Part) for cleavage at 48 hpia. Heat shock had a negative impact (p < .01) on cleavage of IVF embryos, whereas no (p > .05) effect was found in the Part embryos. Embryo development towards blastocyst stage at 168 and 192 hpia decreased in both IVF and Part embryos derived from heat‐shocked oocytes. Heat shock increased (p < .05) the apoptotic index in Part blastocysts, but no effect (p > .05) was found in IVF counterparts. Heat shock also down‐regulated the expression of AQP3 (p < .01) and up‐regulated the expression of HSP70.1 (p < .01) in Part blastocysts, whereas it down‐regulated the expression of ATP1A1 (p < .05) in IVF blastocysts. In conclusion, the effects of heat shock during IVM on early embryo cleavage and blastocyst apoptosis are influenced by the method of oocyte activation and expression of some genes can be disturbed in embryos derived from heat‐shocked oocytes.

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“…[121] In vitro studies, wherein the addition of IGF1 to the culture medium, showed an improvement in the cleavage rate of the bovine oocytes. [122] In human developmental embryo cells, IGF-1 increases GLUT1 expression and stimulates glucose and amino acid uptake. [123] Report indicate that the expression of GLUT and the embryo translocation [124] is regulated by IGF receptors in granulosa cells human and mouse oocytes [125] , also by insulin and IGF-1.…”

Section: Transforming Growth Factor -Beta (Tgf-β)mentioning

confidence: 99%

Role of Cytokines on Fetal Immune Programming

Dubey¹,

Nair²,

Singh³

et al. 2019

Turk J Immunol

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Fetal Immune Programming (FIP) is the reset of the normal fetal development due to the changes in the metabolic environment during critical period in the intrauterine life. Barker's hypothesis states that, uterus is the first environment which the developing fetal immune system encounters. Several reports revealed that intrauterine growth retardation is the cause for increased risk of several non-communicable diseases to the fetus. FIP is connected with maternal immune milieu and hence has a significant impact on the fetal immune system. T-lymphocytes (T-cells) are important for coordinating the immune response and can be characterized into subsets according to their phenotypic characteristics as type-1, type-2 and regulatory T-cells. Each T-cell subset has an exclusive functional role, including their capacity to produce pro-and anti-inflammatory cytokines in response to an immune challenge. Type 1 T cells produce, interferon-γ, interleukin-2 and tumour necrosis factor-α, which promote cellular immune responses, whereas type 2 T cells produce IL-4, IL-5, IL-9, IL10 and IL-13 that provide optimal help for humoral immune responses. Although it is known that T cell cytokines produced in response to fetal molecules could have a role in fetal programming and fetal immune outcomes, the molecular mechanisms underlying the regulation of the immune components at various levels are yet to be elucidated. The present review outlines the role of cytokines on fetal immune programming which would aid in understanding alarmingly increasing incidence of diseases associated with immune dysregulation in the fetus. ÖzCenin bağışıklık sisteminin düzenlenmesi (CBİ), intrauterin hayatta kritik dönem sürecinde metabolik çevredeki değişikliklerden dolayı normal cenin gelişiminin yenilenmesidir. Barker'ın hipotezine göre, uterus, tüm bağışıklık sisteminin ilk geliştiği ortamdır. Bir dizi çalışma, uterus içindeki gelişme yavaşlığının, ceninde bulaşıcı olmayan bazı hastalıkların gelişme olasılığı artırdığını göstermiştir. CBİ, annenin bağışıklık ortamı ile ilişkilidir ve ceninin bağışıklık sistemi üzerinde çok önemli etkisi vardır. T hücreleri, bağışıklık yanıtını düzenlemede etkin hücrelerdir ve tip 1, tip 2 ve düzenleyici T hücreleri olarak ayrı fenotipik gruplara ayrılır. Her bir T hücresi alt grubu yangıyı artıran veya engelleyen sitokinler salgılayarak bağışıklığı etkiler. Tip 1 T hücreleri interferon-γ, interlökin-2 and tümör nekroze edici faktör-α, salınımı ile hücresel bağışıklık yanıtını artırır iken, tip 2 T hücreleri IL-4, IL-5, IL-9, IL10 ve IL-13 salınımı ile sıvısal bağışıklık yanıtını düzenlemede önemli göreve sahiptir. Her ne kadar ceninde üretilen bazı moleküllere yanıt olarak T hücresinden salınan sitokinlerin cenindeki bağışıklık oluşumunda etkili olduğu bilinse de, bu etkinin moleküler mekanizmaları henüz tam olarak ortaya çıkarılamamıştır. Bu derlemede, sitokinlerin ceninin bağışıklığının gelişimindeki rolü ve bu rolün bozulması nedeni ile ortaya çıkan, son yıllarda çok dikkat çekici şekilde artan hastalıklar hakkında ...

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IGF-I slightly improves nuclear maturation and cleavage rate of bovine oocytes exposed to acute heat shockin vitro

Cited by 21 publications

References 51 publications

Thermoprotective effect of insulin-like growth factor 1 on in vitro matured bovine oocyte exposed to heat shock

Thermoprotective effect of insulin-like growth factor 1 on in vitro matured bovine oocyte exposed to heat shock

Contrasting effects of heat shock during in vitro maturation on development of in vitro‐fertilized and parthenogenetic bovine embryos

Role of Cytokines on Fetal Immune Programming

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