Incidence and main causes of infertility in a resident population (1 850 000) of three French regions (1988–1989)*

Thonneau, Patrick; Marchand, Sophie; Tallec, A.; Ferial, Marie-Laure; Ducot, B.; Lansac, J.; Lopès, P.; Tabaste, Jean-Marie; Spira, Alfred

doi:10.1093/oxfordjournals.humrep.a137433

Cited by 742 publications

(477 citation statements)

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“…The field of sperm biology and pathophysiology is certainly one of the least developed in reproduction research. However, male infertility because of sperm dysfunction (1 in 15 men) (57) and a general decrease in male fertility are growing areas in the field. To understand the underlying mechanisms involved in sperm dysfunction, one should first decipher the normal biochemical mechanisms of its functions.…”

Section: Discussionmentioning

confidence: 99%

Identification of Extracellular Signal-regulated Kinase 1/2 and p38 MAPK as Regulators of Human Sperm Motility and Acrosome Reaction and as Predictors of Poor Spermatozoan Quality

Almog

Lazar

Reiss

et al. 2008

Journal of Biological Chemistry

110

127

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Mature spermatozoa acquire progressive motility only after ejaculation. Their journey in the female reproductive tract also includes suppression of progressive motility, reactivation, capacitation, and hyperactivation of motility (whiplash), the mechanisms of which are obscure. MAPKs are key regulatory enzymes in cell signaling, participating in diverse cellular functions such as growth, differentiation, stress, and apoptosis. Here we report that ERK1/2 and p38 MAPK are primarily localized to the tail of mature human spermatozoa. Surprisingly, c-Jun N-terminal kinase 1/2, which is thought to be ubiquitously expressed, could not be detected in mature human spermatozoa. ERK1/2 stimulation is downstream to protein kinase C (PKC) activation, which is also present in the human sperm tail (PKC␤I and PKC⑀). ERK1/2 stimulates and p38 inhibits forward and hyperactivated motility, respectively. Both ERK1/2 and p38 MAPK are involved in the acrosome reaction. Using a proteomic approach, we identified ARHGAP6, a RhoGAP, as an ERK substrate in PMA-stimulated human spermatozoa. Inverse correlation was obtained between the relative expression level of ERK1 or the relative activation level of p38 and sperm motility, forward progression motility, sperm morphology, and viability. Therefore, increased expression of ERK1 and activated p38 can predict poor human sperm quality.

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Section: Discussionmentioning

confidence: 99%

Identification of Extracellular Signal-regulated Kinase 1/2 and p38 MAPK as Regulators of Human Sperm Motility and Acrosome Reaction and as Predictors of Poor Spermatozoan Quality

Almog

Lazar

Reiss

et al. 2008

Journal of Biological Chemistry

110

127

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“…Ces donn6es se sont vues globalement confirm6es par une 6tude plus r6cente [56] portant sur 1686 couples de 3 d6partements fran~ais. La pr4valence de l'inf6condit6 est de 14,1%, ce qui, extrapol6 ~ la population fran~aise, repr6-sente 60 000 couples venant consulter chaque ann6e.…”

Section: Importance De La Demande De Soins Pour Infertilit4 De Coupleunclassified

“…Des r6sultats assez similaires se retrouvent dans l'enqu~te fran~aise plus r6cente [56], un facteur masculin existe dans au moins 20 + 39 = 59 % des cas d'infertilit4 de couple. Facteur f4minin pr6dominant 35 44 40 29 29 35 33 Facteur masculin pr4dominant 25 9 15 25 22 20 20 Associations de facteurs masculins et f6minins 24 41 29 34 45 35 39 Cause ind4termin4e 16 6 15 11 4 10 8 l0 On peut sch4matiquement distinguer deux grands cadres physiopathologiques :…”

Section: L'infertilit4 De Couple Est Partag4eunclassified

Overview of male infertility

Lejeune

1999

Androl.

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RI~SUMI~Cette revue fait le point sur l'dpid4miolo-gie, l'~tiologie et la th4rapeutique de l'infertilit4 masculine en insistant sur les donn4es nouvelles. Le progr~s th4rapeu-tique majeur que constitue la microinjection amine h consid4rer les causes d'infertilit4 masculine en fonction de l'4tat de sant4 des enfants qui seront obtenus. Les 4tudes concernant l'intervention possible de x4nobiotiques perturbant le contr61e hormonal des fonctions testiculaires sont en cours. Des causes g4n4-tiques d'infertilit4 ont ~t4 identifi4es, il s'agit d'une part des microd414tions du bras long du chromosome Y responsables d'une part non n4gligeable de troubles de la spermatog4n~se, et d'autre part d'alt4-ration du g~ne CFRT faisant de l'ag4n4-sie v4siculo-d4f4rentielle une forme fruste de mucoviscidose. Ces anomalies g4n4-tiques ainsi que les anomalies chromosomiques, classiquement reconnues comme responsables de troubles de la spermatog4n~se, ont des implications dans la possible transmission de troubles de la reproduction, voire de pathologies plus g4n4rales, aux enfants qui peuvent ~tre obtenus grfice h la microinjection de spermatozoides recueillis dans l'4jaculat, les voies excr4trices ou le testicule luims

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“…Infertility is estimated to affect up to 15 % of couples of reproductive age [2]. The causes of infertility are variable; they can be of male (20 %), female (34 %), mixed (38 %) or even idiopathic (8 %) origins [3].…”

Section: Introductionmentioning

confidence: 99%

Genetic aspects of monomorphic teratozoospermia: a review

Braekeleer

Nguyen

Morel

et al. 2015

J Assist Reprod Genet

113

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Teratozoospermia is characterized by the presence of spermatozoa with abnormal morphology over 85 % in sperm. When all the spermatozoa display a unique abnormality, teratozoospermia is said to be monomorphic. Two forms of monomorphic teratozoospermia, representing less than 1 % of male infertility, are recognized: macrozoospermia (also called macrocephalic sperm head syndrome) and globozoospermia (also called round-headed sperm syndrome). Macrozoospermia is defined as the presence of a very high percentage of spermatozoa with enlarged head and multiple flagella. Meiotic segregation studies in 30 males revealed that over 90 % of spermatozoa were aneuploid, mainly diploid. Sperm DNA fragmentation studies performed in a few patients showed an increase in DNA fragmentation index compared to fertile men. Four mutations in the AURKC gene, a key player in meiosis and more particularly in spermatogenesis, have been found to be responsible for macrozoospermia. Globozoospermia is characterized by round-headed spermatozoa with an absent acrosome, an aberrant nuclear membrane and midpiece defects. The rate of aneuploidy of various chromosomes in spermatozoa from 26 globozoospermic men was slightly increased compared to fertile men. However, this increase was of the same order as that commonly found in infertile men with altered sperm parameters. The majority of the studies found that globozoospermic males had a sperm DNA fragmentation index higher than in fertile men. Mutations or deletions in three genes, SPATA16, PICK1 and DPY19L2, have been shown to be responsible for globozoospermia. Identification of the genetic causes of macrozoospermia and globozoospermia should help refine diagnosis and treatment of these patients, avoiding long and painful treatments. Elucidating the molecular causes of these defects is of utmost importance as intracytoplasmic sperm injection (ICSI) is very disappointing in these two pathologies.

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Incidence and main causes of infertility in a resident population (1 850 000) of three French regions (1988–1989)*

Cited by 742 publications

References 0 publications

Identification of Extracellular Signal-regulated Kinase 1/2 and p38 MAPK as Regulators of Human Sperm Motility and Acrosome Reaction and as Predictors of Poor Spermatozoan Quality

Identification of Extracellular Signal-regulated Kinase 1/2 and p38 MAPK as Regulators of Human Sperm Motility and Acrosome Reaction and as Predictors of Poor Spermatozoan Quality

Overview of male infertility

Genetic aspects of monomorphic teratozoospermia: a review

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