Table 1 Pten knockout mice
From: Role of PTEN-less in cardiac injury, hypertrophy and regeneration
Conventional Knockout | ||||||
Pten Exons | Target cells | Effect | Years | Ref. | ||
Exons 3–5 | ES cells | Embryonic lethality | 1998 | (Suzuki et al. 1998) | ||
Exons 4–5 | ES cells | Embryonic lethality | 1998 | (Di Cristofano et al. 1998) | ||
Conditional Knockout | ||||||
Floxed Exons | Tissue specific deletion | |||||
Pten Exons | Ref. | Cre | Target cells | Effect | Years | Ref. |
Exons 4–5 | (Suzuki et al. 2001) | Lck-Cre | T cells | Pten knockout T cells are autoreactive, hyperproliferate, resist apoptosis and secreate high level Th1/Th2 cytokines, show increased p-PKB/Akt and p-ERK | 2001 | (Suzuki et al. 2001) |
Exons 4–5 | Gfap-Cre | Brain glial cells | Mice showed enlarged brain and developed seizures and ataxia by 9 weeks and died by 29 weeks, Pten mutant cells shoewed an increased soma size and elevated p-Akt | 2001 | (Backman et al. 2001) | |
Exons 4–5 | Mck-Cre | Skeletal and cardiac muscle | Knockou Pten induced heart hypertrophy without pathlogical change and decreaed heart contractility through mediating PI3Kγ | 2002 | (Crackower et al. 2002) | |
Exons 4–5 | Alb-Cre | Hepatocyte | Mice showed massive hepatomegaly and steatohepatitis with triglyceride accumulation, hepatocytes showed hyperproliferation and abnormal activation of protein kinase B and MAPK | 2004 | (Horie et al. 2004) | |
Exons 4–5 | Nse-Cre | Differentiated neurons in the cerebral cortex and hippocampus | Mice showed abnormal social interaction and exaggerated responses to sensory stimuli, with activation of the Akt/ mTor/S6k pathway and inactivation of Gsk3β | 2006 | (Kwon et al. 2006) | |
Exons 4–5 | Mck-Cre | Skeletal and cardiac muscle | Mice showed reduced pathological hypertrophy, less interstitial fibrosis, reduced apoptosis and marked preservation of LV function in aortic banding induced pressure overload model, and markedly reduced p-JNK1,p-JNK2 and p-p38 | 2008 | (Oudit et al. 2008) | |
Exons 4–5 | SM22α-Cre | Smooth muscle cells | Mice shopwed widespread medial SMC hyperplasia, vascular remodeling, and histopathology consistent with pulmonary hypertension | 2008 | (Nemenoff et al. 2008) | |
Exons 4–5 | PdgfbiCreERT2 (Cre induced by tamoxifen) | Endothelial cell | Endothelial deletion of PTEN results in vascular hyperplasia because cannot regulate Notch-induced proliferation arrest. Both the catalytic and non-catalytic APC/C-Fzr1/Cdh1-mediated activities of PTEN are required for stalk cells’ proliferative arrest | 2015 | (Serra et al. 2015) | |
Exon 5 | Nestin-Cre | Central nervous system stem/progenitor cells | Mice deletion PTEN showed enlarged and abnormal brains, with increased cell proliferation, decreased cell death, and enlarged cell size | 2001 | (Groszer et al. 2001) | |
Exon 5 | ARR2Probasin-Cre | Prostatic epithelial cells | Pten deletion successfully induced murine prostate cancer model | 2003 | (Wang et al. 2003) | |
Exon 5 | Mx-1-Cre (Cre induced by polyinosine-polycytidine) | Bone marrow Haematopoietic stem cells (HSCs) | The ability of sustain haematopoietic reconstitution affected in Pten-deicient HSCs, mice with Pten deletion showed an increased representation of myeloid and T-lymphoid lineages and develop myeloproliferative disorder | 2006 | (Zhang et al. 2006) | |
Exon 5 | Gdf-9-Cre | Oocytes | Lacking PTEN in oocytes activated the entire primordial folliclepool and caused premature ovarian failure | 2008 | (Reddy et al. 2008) | |
Exon 5 | α-MHC-MerCreMer (Cre induced by tamoxifen) | Cardiomyocytes | PtenCKO hearts exhibited increased PI3K activity in baseline,and better function recovery after ischemia/reperfusion,with fewer apoptosis and higher level of ERK and BCL-2 expression | 2009 | (Ruan et al. 2009) | |
Exon 5 | AAV- Cre | Corticospinal neurons | Deletion PTEN enhanced compensatory sprouting of of uninjured corticospinal tract axons and enabled regeneration of a cohort of injured corticospinal tract axons past a spinal cord lesion | 2010 | (Liu et al. 2010) | |
Exon 5 | Pax7CreER | Quiescent satellite cells | Quiescent satellite cells specific knockout Pten lead to spontaneous activation and premature differentiation and resulted in failed regeneration. Mechanistically, Pten deletion increases Akt phosphorylation, further induced FoxO1 cytoplasmic translocation and Notch signalling suppression | 2017 | (Yue et al. 2017) | |
Exon 5 | α-MHC-MerCreMer (Cre induced by tamoxifen) | Cardiomyocytes | Cardiac-specific knockout Pten in adult mice preserved heart function, decreased scar size and promoted cariomyocytes proliferation after myocardial infarction stress | 2020 | (Liang et al. 2020) | |