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Updated: May 23, 2026
A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
CD147 regulates apoptosis in mouse spermatocytes but not spermatogonia
Hao Chen1, Kin Lam Fok, Xiaohua Jiang
1Department of Gynaecology, The Second People's Hospital of Shenzhen, Shenzhen, People's Republic of China.
Background:
Spermatogenesis is maintained by a dynamic balance between germ cell proliferation and apoptosis. Previous study has demonstrated that CD147 knockout mice are infertile with arrested germ cells. However, the question of whether and how CD147 may be involved in the apoptotic process during spermatogenesis remains elusive. The aim of this study was to evaluate the role of CD147 in the regulation of germ cell apoptosis in mice.
Methods:
CD147 function was blocked by anti-CD147 antibody in GC-1 (immortalized spermatogonia) and GC-2 (immortalized spermatocytes) cell lines and in testicular germ cells in vivo. Testes size and weight were examined after injection of anti-CD147 antibody into the seminiferous tubules of severe combined immunodeficiency mice. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and levels of p53 and two effectors, caspase 3 and poly ADP-ribose polymerase (PARP), using western blots.
Results:
The size and weight of the CD147-immunodepleted testes were decreased compared with that in control testes (P < 0.001). The TUNEL assay showed an increase in the number of apoptotic spermatocytes (P < 0.001 versus control) but not spermatogonia in Stages XI-XII of CD147-immunodepleted testes. In addition, in vitro experiments demonstrated that CD147 immunodepletion induced an increase in apoptosis in GC-2 cells (P < 0.001 versus control) but had no effect on GC-1 cells. Moreover, deprivation of CD147 induced apoptosis in spermatocytes through a p53-independent mechanism, which led to caspase 3 and PARP activation.
Conclusions:
We have demonstrated that immunodepletion of CD147 induces p53-independent apoptosis in mouse spermatocytes but not spermatogonia.
Insights
Blocking CD147 (basigin) protein in mice induces apoptosis in spermatocytes, not spermatogonia. This p53-independent mechanism affects caspase activation, impacting male fertility.
Area of Science:
- Reproductive Biology
- Cell Biology
- Molecular Biology
Background:
- Spermatogenesis relies on a balance between germ cell proliferation and apoptosis.
- CD147 knockout mice exhibit infertility and germ cell arrest.
- The role of CD147 in germ cell apoptosis during spermatogenesis is not well understood.
Purpose of the Study:
- To investigate the role of CD147 in regulating germ cell apoptosis in mice.
- To determine if CD147 influences the apoptotic process in spermatogenesis.
Main Methods:
- CD147 function was inhibited using an anti-CD147 antibody in cell lines (GC-1, GC-2) and in vivo.
- Testicular germ cell apoptosis was assessed via TUNEL assay and Western blotting for p53, caspase 3, and PARP.
- Changes in testes size and weight were measured after antibody injection.
Main Results:
- CD147 immunodepletion led to decreased testes size and weight.
- An increase in apoptotic spermatocytes, but not spermatogonia, was observed in CD147-depleted testes.
- In vitro, CD147 depletion induced apoptosis in spermatocyte-derived GC-2 cells but not in spermatogonia-derived GC-1 cells.
Conclusions:
- CD147 immunodepletion triggers apoptosis in mouse spermatocytes via a p53-independent pathway.
- This apoptosis involves the activation of caspase 3 and PARP.
- CD147 does not appear to regulate apoptosis in spermatogonia.
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