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Written | Edited by Wang Cong | Typeset by Wang Duoyu | Shuichengwen male infertility is a multifactorial heterogeneous disease that affects approximately 7% of men
.
Non-obstructive azoospermia (NOA) is one of the most serious male reproductive system diseases.
It refers to the inability of testicular tissue to produce sperm.
About 1% of men of childbearing age will suffer from this disease
.
On January 3, 2022, Gao Fei, a researcher from the Institute of Zoology, Chinese Academy of Sciences, and Professor Li Zheng from the Urology Center of the First People’s Hospital Affiliated to Shanghai Jiaotong University, etc.
published a title in the journal Signal Transduction and Targeted Therapy: Oligomer-Targeting Prevention of Neurodegenerative Dementia by Intranasal Rifampicin and Resveratrol Combination – A Preclinical Study in Model Mice
.
The study revealed that MSH5 gene mutation is a potential cause of non-obstructive azoospermia (NOA), and confirmed in mouse models that CRISPR/Cas9 gene editing can repair the gene mutation and produce mature sperm
.
The paper studied three non-obstructive azoospermia (NOA) patients (numbered P8944, P7602, P7824), and the three of them came from three Chinese families with no history of fertility problems
.
First, the research team ruled out known causes of male infertility, including cryptorchidism, hypogonadism, cancer, alcohol and smoking
.
Their reproductive system is also normally developed, and their testicular size and FSH hormone levels are relatively normal
.
Further examination showed that they did not have chromosomal abnormalities
.
In order to further determine the cause of the infertility of these three patients, the research team performed full-exome gene sequencing on them
.
The MSH5 gene of the P8944 patient has a four-base deletion homozygous mutation, which causes the stop codon to be advanced, and the protein expressed by MSH5 is missing 587 amino acids
.
His parents and siblings carry a mutation, so they are not sick
.
The P7602 and P7824 patients are in the same situation.
They both have compound heterozygous mutations in the MSH5 gene, which means that their two MSH5 alleles have mutations, but the mutation sites are different
.
The four mutation sites in these three patients are highly conserved among different species
.
In order to verify the function of the MSH5 gene mutation, the research team conducted studies on mice.
The testes of male mice carrying the MSH5 gene homozygous mutation were significantly smaller, and a large number of apoptotic cells appeared in the seminiferous tubules
.
This suggests that MSH5 mutation may be one of the causes of non-obstructive azoospermia (NOA)
.
However, the testes of these three patients were relatively normal, which may be due to the different effects of the MSH5 gene in humans and mice
.
The CRISPR/Cas9 system is currently the most powerful gene editing technology, and it has been widely used in animal disease models and human treatments
.
In order to save the aforementioned MSH5 gene mutant mice, the research team injected CRISPR gene editing components (sgRNA, Cas9-expressing plasmid, MSH5 gene single-stranded DNA template) or MSH5 gene plasmid into the mouse seminiferous tubules
.
After injection, electroporation was used to improve the transfection efficiency.
After 5 weeks, a small amount of mature sperm with head and tail was found in the seminiferous tubules of these mice
.
However, no mature sperm were found in the tail of the epididymis, which may be due to the low gene editing efficiency of this system
.
Further research is needed to improve transfection efficiency and editing effect
.
In general, the study shows that MSH5 gene mutation is a potential cause of non-obstructive azoospermia (NOA).
It is important to balance that the study repaired the MSH5 gene mutation in the mouse model through in vivo gene editing, which suggests This method has the potential to treat male reproductive system diseases
.
Link to the paper: https:// open for reprinting, welcome to forward to Moments and WeChat groups
.
Non-obstructive azoospermia (NOA) is one of the most serious male reproductive system diseases.
It refers to the inability of testicular tissue to produce sperm.
About 1% of men of childbearing age will suffer from this disease
.
On January 3, 2022, Gao Fei, a researcher from the Institute of Zoology, Chinese Academy of Sciences, and Professor Li Zheng from the Urology Center of the First People’s Hospital Affiliated to Shanghai Jiaotong University, etc.
published a title in the journal Signal Transduction and Targeted Therapy: Oligomer-Targeting Prevention of Neurodegenerative Dementia by Intranasal Rifampicin and Resveratrol Combination – A Preclinical Study in Model Mice
.
The study revealed that MSH5 gene mutation is a potential cause of non-obstructive azoospermia (NOA), and confirmed in mouse models that CRISPR/Cas9 gene editing can repair the gene mutation and produce mature sperm
.
The paper studied three non-obstructive azoospermia (NOA) patients (numbered P8944, P7602, P7824), and the three of them came from three Chinese families with no history of fertility problems
.
First, the research team ruled out known causes of male infertility, including cryptorchidism, hypogonadism, cancer, alcohol and smoking
.
Their reproductive system is also normally developed, and their testicular size and FSH hormone levels are relatively normal
.
Further examination showed that they did not have chromosomal abnormalities
.
In order to further determine the cause of the infertility of these three patients, the research team performed full-exome gene sequencing on them
.
The MSH5 gene of the P8944 patient has a four-base deletion homozygous mutation, which causes the stop codon to be advanced, and the protein expressed by MSH5 is missing 587 amino acids
.
His parents and siblings carry a mutation, so they are not sick
.
The P7602 and P7824 patients are in the same situation.
They both have compound heterozygous mutations in the MSH5 gene, which means that their two MSH5 alleles have mutations, but the mutation sites are different
.
The four mutation sites in these three patients are highly conserved among different species
.
In order to verify the function of the MSH5 gene mutation, the research team conducted studies on mice.
The testes of male mice carrying the MSH5 gene homozygous mutation were significantly smaller, and a large number of apoptotic cells appeared in the seminiferous tubules
.
This suggests that MSH5 mutation may be one of the causes of non-obstructive azoospermia (NOA)
.
However, the testes of these three patients were relatively normal, which may be due to the different effects of the MSH5 gene in humans and mice
.
The CRISPR/Cas9 system is currently the most powerful gene editing technology, and it has been widely used in animal disease models and human treatments
.
In order to save the aforementioned MSH5 gene mutant mice, the research team injected CRISPR gene editing components (sgRNA, Cas9-expressing plasmid, MSH5 gene single-stranded DNA template) or MSH5 gene plasmid into the mouse seminiferous tubules
.
After injection, electroporation was used to improve the transfection efficiency.
After 5 weeks, a small amount of mature sperm with head and tail was found in the seminiferous tubules of these mice
.
However, no mature sperm were found in the tail of the epididymis, which may be due to the low gene editing efficiency of this system
.
Further research is needed to improve transfection efficiency and editing effect
.
In general, the study shows that MSH5 gene mutation is a potential cause of non-obstructive azoospermia (NOA).
It is important to balance that the study repaired the MSH5 gene mutation in the mouse model through in vivo gene editing, which suggests This method has the potential to treat male reproductive system diseases
.
Link to the paper: https:// open for reprinting, welcome to forward to Moments and WeChat groups
