Role of Neutrophils in Matrix Metalloproteinase Activity in the Preimplantation Mouse Uterus1

Daimon, Etsuko; Wada, Yoshinao

doi:10.1095/biolreprod.104.038539

Cited by 34 publications

(19 citation statements)

References 35 publications

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“…In our experiments, we detected only the latent form of MMP-9 (pro MMP-9) in the gelatin zymography. Regarding MMP-9, it has been reported that MMP-9 is not always detected in many tissues in vivo, although pro MMP-9 is converted to MMP-9 by various protease such as MMP-1, MMP-2, MMP-3 or plasminogen activator in vitro [54]. In addition, MMP-9 activation locally occurs in a pericellular environment by inflammatory response, leaving much of the secreted MMP in its pro-form [55].…”

Section: Discussionmentioning

confidence: 99%

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ)

Fukushima

Nakamura

Ueda

et al. 2007

BMC Musculoskelet Disord

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Background: Matrix metalloproteinases (MMPs) are key regulatory molecules in the formation, remodeling and degradation of all extracellular matrix (ECM) components in both physiological and pathological processes in various tissues. The aim of this study was to examine the involvement of gelatinase MMP family members, MMP-2 and MMP-9, in dystrophin-deficient skeletal muscle. Towards this aim, we made use of the canine X-linked muscular dystrophy in Japan (CXMD J ) model, a suitable animal model for Duchenne muscular dystrophy.

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Section: Discussionmentioning

confidence: 99%

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ)

Fukushima

Nakamura

Ueda

et al. 2007

BMC Musculoskelet Disord

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“…Neutrophils have been identified as the key source of MMP-9, a collagen specific protease during the peri-implantation period [93], while macrophages are known to produce a range of MMPs. A comprehensive study by Chow et al [94] in the golden hamster showed that expression of molecules involved in ECM remodelling are controlled in a temporal and spatial manner and that seminal plasma is implicated in their regulation.…”

Section: Tissue Remodelling and Seminal Plasmamentioning

confidence: 99%

Seminal fluid and reproduction: much more than previously thought

Bromfield

2014

J Assist Reprod Genet

127

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The influence of seminal plasma on the cytokine and immune uterine environment is well characterised in mice and humans, while the effects of disruption to uterine seminal plasma exposure on pregnancy and offspring health is becoming more clearly understood. The cellular and molecular environment of the uterus during the pre-and peri-implantation period of early pregnancy is critical for implantation success and optimal foetal and placental development. Perturbations to this environment not only have consequences for the success of pregnancy and neonatal health and viability, but can also drive adverse health outcomes in the offspring after birth, particularly the development of metabolic disorders such as obesity, hypertension and insulin resistance. It is now reported that an absence of seminal plasma at conception in mice promotes increased fat accumulation, altered metabolism and hypertension in offspring. The evidence reviewed here demonstrates that seminal plasma is not simply a transport medium for sperm, but acts also as a key regulator of the female tract environment providing optimal support for the developing embryo and benefiting future health of offspring.

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“…In addition to serine proteases, other proteases like MMPs are also capable of degrading extracellular matrix proteins. Although MMP proteins do not possess the catalytic triads required for proteolytic function in KLKs (His57, Asp102, and Ser195) [42], neutrophils bearing proMMP9 can be attracted by seminal plasma and their activities are elevated post-coitus in the female uterus [43]. In our model, all Mmp transcripts and their inhibitors were expressed at the same level between Esr1 f/f and Wnt7a Cre/+ ; Esr1 f/f uteri.…”

Section: Discussionmentioning

confidence: 99%

Crucial role of estrogen for the mammalian female in regulating semen coagulation and liquefaction in vivo

García

Gewiss

et al. 2017

PLoS Genet

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Semen liquefaction changes semen from a gel-like to watery consistency and is required for sperm to gain mobility and swim to the fertilization site in the Fallopian tubes. Kallikrein-related peptidases 3 (KLK3) and other kallikrein-related peptidases from male prostate glands are responsible for semen liquefaction by cleaving gel-forming proteins (semenogelin and collagen). In a physiological context, the liquefaction process occurs within the female reproductive tract. How seminal proteins interact with the female reproductive environment is still largely unexplored. We previously reported that conditional genetic ablation of Esr1 (estrogen receptor α) in the epithelial cells of the female reproductive tract (Wnt7a) causes female infertility, partly due to a drastic reduction in the number of motile sperm entering the oviduct. In this study, we found that post-ejaculated semen from fertile wild-type males was solidified and the sperm were entrapped in Wnt7aCre/+ ;Esr1 f/f uteri, compared to the watery semen (liquefied) found in Esr1 f/f controls. In addition, semenogelin and collagen were not degraded in Wnt7aCre/+ ;Esr1 f/f uteri. Amongst multiple gene families aberrantly expressed in the absence of epithelial ESR1, we have identified that a lack of Klks in the uterus is a potential cause for the liquefaction defect. Pharmacological inhibition of KLKs in the uterus replicated the phenotype observed in Wnt7aCre/+ ;Esr1 f/f uteri, suggesting that loss of uterine and seminal KLK function causes this liquefaction defect. In human cervical cell culture, expression of several KLKs and their inhibitors (SPINKs) was regulated by estrogen in an ESR1-dependent manner. Our study demonstrates that estrogen/ESR1 signaling in the female reproductive tract plays an indispensable role in normal semen liquefaction, providing fundamental evidence that exposure of post-ejaculated semen to the suboptimal microenvironment in the female reproductive tract leads to faulty liquefaction and subsequently causes a fertility defect. Author summarySemen liquefaction has been considered to be solely modulated by prostate-derived kallikrein-related peptidases (KLKs), especially KLK3 (or prostate specific antigen). However, our research demonstrated that female mice lacking estrogen receptor alpha (ERα) in the uterine epithelial cells had a drastic decrease in Klk transcripts and semen from fertile males fails to liquefy within the uteri of these females. Therefore, our results provide a novel aspect that, due to an interplay between semen and female reproductive tract secretions, the physiology of semen liquefaction is more complicated than previously assumed. This information will advance research on semen liquefaction in the female reproductive tract, an area that has never been explored, and could lead to the development of diagnostic tools for unexplained infertility cases and non-invasive contraception technologies.

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Role of Neutrophils in Matrix Metalloproteinase Activity in the Preimplantation Mouse Uterus1

Cited by 34 publications

References 35 publications

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ)

Activation and localization of matrix metalloproteinase-2 and -9 in the skeletal muscle of the muscular dystrophy dog (CXMDJ)

Seminal fluid and reproduction: much more than previously thought

Crucial role of estrogen for the mammalian female in regulating semen coagulation and liquefaction in vivo

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