Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: Islet PTEN upregulation with concomitant attenuation of PI3K signaling in models of type 2 diabetes. A and B : PTEN transcript levels by quantitative PCR ( A ) and immunohistochemical staining ( B ) of chow- and HFD-fed (after 7 months on HFD); wild-type (+/+) and db/db islets (7 months of age) ( n = 3). C : Western blot (left panel) and quantification ( right panel ) of PTEN, p-Akt (Ser473), total Akt, p-mTOR (Ser2448), total mTOR, p-FoxO-1 (Ser253) and total FoxO-1 in chow- and HFD-fed (7 months on HFD); wild-type and db/db islets (7 months of age) ( n = 3). * P < 0.05; ** P < 0.005. Scale bar, 50 μm. The results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Real-time Polymerase Chain Reaction, Immunohistochemical staining, Staining, Western Blot

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: PTEN deletion in RIP cre + Pten fl/fl islets. A : Immunohistochemical staining of PTEN in RIP cre + Pten +/+ (+/+) and RIP cre + Pten fl/fl (−/−) pancreas sections. B : Western blot ( left panel ) and quantification ( right panel ) of PTEN expression in RIP cre + Pten fl/fl islets and hypothalamus (Hyp) ( n = 3). * P < 0.05; ** P < 0.005. Scale bar, 50 μm. The results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Immunohistochemical staining, Staining, Western Blot, Expressing

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: RIP cre + Pten fl/fl mice showed maintained glucose metabolism and in vivo glucose stimulated insulin secretion after prolonged HFD while demonstrating drastic weight gain. A : Weight of RIP cre + Pten +/+ (+/+) and RIP cre + Pten fl/fl (−/−) mice at the start of HFD (2 months of age) and after HFD (9 months of age) with chow-fed RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice at the same time points. B : Fasting blood glucose of RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice fed either chow or HFD for 7 months ( n >7). C : Glucose tolerance tests of RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice after 7 months of either chow or HFD feeding ( n >7). D : in vivo glucose stimulated insulin secretions of RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice after 7 months of either chow or HFD feeding ( n >3). * P < 0.05. The results are presented as mean ± SE.

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: In Vivo

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: RIP cre + Pten fl/fl mice maintained high islet mass and β-cell size with protection against HFD-induced β-cell dysfunction. A and B : Insulin staining ( A ) and quantification ( B ) of pancreas sections of RIP cre + Pten +/+ (+/+) and RIP cre + Pten fl/fl (−/−) mice fed either chow or HFD ( n = 3), Scale bar, 500 μm. C : Percentage of Ki67 positive cells in islets from RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice fed either chow or HFD ( n = 3). D : proportion of small (<10 cells), medium (10–200 cells) and large (>200 cells) islet in pancreas from RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice fed either chow or HFD ( n = 3). E and F : Immunofluorescent staining of insulin/DAPI ( E ) and quantification of β-cell size ( F ) of pancreas from RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice fed either chow or HFD ( n = 3), Scale bar, 50 μm. G and H : Insulin secretion per 60 islets during perifusion analysis ( G ) and quantification of area under the curve (AUC) ( H ) of chow-fed RIP cre + Pten +/+ and RIP cre + Pten fl/fl islets ( n = 3). I and J : Insulin secretion per 60 islets during perifusion analysis ( I ) and quantification of area under the curve ( J ) of HFD-fed RIP cre + Pten +/+ and RIP cre + Pten fl/fl islets ( n = 3). * P < 0.05. Results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Staining

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: RIP cre + Pten fl/fl mice maintained islet PI3K signaling after prolonged HFD. A : Immunofluorescent staining of insulin/glucagon, and immunohistochemical staining of p-Akt (Ser473), total Akt, GLUT2, and PDX-1 in chow-fed, HFD-fed RIP cre + Pten +/+ (+/+) and HFD-fed RIP cre + Pten fl/fl (−/−) mice. B : Western blot ( left panel ) and quantification ( right panel ) of p-Akt (Ser473), total Akt, p-mTOR (Ser2448), total mTOR, p-FoxO-1 (Ser253), total FoxO-1, GLUT-2, and PDX-1 of islets from RIP cre + Pten +/+ and RIP cre + Pten fl/fl mice fed either chow or HFD ( n = 3). * P < 0.05. Scale bar, 50 μm. Results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Staining, Immunohistochemical staining, Western Blot

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: RIP cre + Pten fl/fl Lepr db/db mice exhibited comparable weight gain and normal glucose tolerance despite being insulin resistant with normal β-cell function. A : Weight of wild-type (WT), RIP cre + Pten +/+ Lepr db/db ( db/db ), and RIP cre + Pten fl/fl Lepr db/db (−/−; db/db ) mice at 2 and 7 months of age ( n >7). B : Fed blood glucose of wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice from 2 to 7 months of age ( n >7). C : Glucose tolerance test of wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice at 7 months of age ( n >7). D : Insulin tolerance test of wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice at 7 months of age ( n >7). E : In vivo glucose-stimulated insulin secretion of wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice at 7 months of age ( n = 3). F and G : Insulin secretion per 60 islets during perifusion analysis ( F ) and quantification of area under the curve ( G ) of wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice ( n = 3). * P < 0.05 for RIP cre + Pten fl/fl Lepr db/db mice compared with RIP cre + Pten +/+ Lepr db/db mice or as indicated; φ P < 0.05 for both RIP cre + Pten +/+ Lepr db/db and RIP cre + Pten fl/fl Lepr db/db mice compared with wild-type mice. Results are presented as mean ± SE.

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Cell Function Assay, In Vivo

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: RIP cre + Pten fl/fl Lepr db/db mice exhibit islet hypertrophy with normal islet architecture and enhanced PI3K signaling. A : Immunofluorescent staining of insulin/glucagon, and immunohistochemical staining of synaptophysin, p-Akt (Ser473), total Akt, GLUT2, and PDX-1 in wild-type (WT), RIP cre + Pten +/+ Lepr db/db ( db/db ), and RIP cre + Pten fl/fl Lepr db/db (−/−; db/db ) mice at 7 months of age. B : Quantification of islet area in wild type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db at 7 months of age ( n = 4). C : Percentage of Ki67 positive cells in wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice at 7 months of age ( n = 4). D : Western blot ( left panel ) and quantification ( right panel ) of p-Akt (Ser473), total Akt, p-mTOR (Ser2448), total mTOR, p-FoxO-1 (Ser253), total FoxO-1, GLUT-2, and PDX-1 of islets from wild-type, RIP cre + Pten +/+ Lepr db/db , and RIP cre + Pten fl/fl Lepr db/db mice at 7 months of age ( n = 3). * P < 0.05. Scale bar, 500 μm ( A , top panel ); 50 μm ( A, rows 2 to 6 ). Results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Staining, Immunohistochemical staining, Western Blot

Journal: Diabetes

Article Title: Deletion of Pten in Pancreatic β-Cells Protects Against Deficient β-Cell Mass and Function in Mouse Models of Type 2 Diabetes

doi: 10.2337/db09-1805

Figure Lengend Snippet: HFD-fed RIP cre + Pten fl/fl and RIP cre + Pten fl/fl Lepr db/db mice showed intact islet integrity and uncompromised response to gamma irradiation. A : Laminin and β-catenin staining demonstrated intact basement membrane and cell-to-cell adhesion in HFD-fed (9 months of age) RIP cre + Pten fl/fl (−/−) and RIP cre + Pten fl/fl Lepr db/db (−/−; db/db ) (9 months of age) mice. B : Transcripts levels of p53-related gene including Bax , Mdm2 , and p21 during quantitative PCR of RIP cre + Pten +/+ (+/+) and RIP cre + Pten fl/fl islets with or without 30Gy gamma irradiation ( n = 2). C : Western blotting ( left panel ) and quantification ( right panel ) of p-p53 (Ser392), total p53, cleaved MDM2, and total MDM2 in RIP cre + Pten +/+ and RIP cre + Pten fl/fl islets with or without 30Gy gamma irradiation ( n = 2). * P < 0.05. Scale bar, 50 μm. Results are presented as mean ± SE. (A high-quality digital representation of this figure is available in the online issue.)

Article Snippet: For immunohistochemical and immunofluorescent staining antibodies against PTEN (NeoMarker, Fremont, CA), Akt (Cell Signaling Technology, Beverly, MA), p-Akt (Ser473) (Cell Signaling Technology, Beverly, MA), insulin (DAKO), glucagon (NovoCastra Laboratories), laminin (Sigma), β-catenin (BD Transduction Laboratories), GLUT2 (Chemicon, Temecula, CA), PDX-1 (Chemicon, Temecula, CA), and Ki67 (DAKO) were used.

Techniques: Irradiation, Staining, Membrane, Real-time Polymerase Chain Reaction, Western Blot

Journal: The American Journal of Pathology

Article Title: N -Acetylcysteine Resolves Placental Inflammatory-Vasculopathic Changes in Mice Consuming a High-Fat Diet

doi: 10.1016/j.ajpath.2019.07.010

Figure Lengend Snippet: Increased IL-1β immunoreactivity in labyrinth of vehicle high-fat diet (HFD) (HFDVeh) placenta is ameliorated with N-acetylcysteine (NAC) treatment. A and B: Minimal immunohistochemical staining of IL-1β in labyrinth of vehicle control (CtrlVeh) (A) and NAC control (CtrlNAC) (B) placentas. C and D: Increased IL-1β in HFDVeh labyrinth (C) is reduced to control levels by NAC treatment (D). E: Box and whisker plot of IL-1β immunoreactivity. n = 6 per group. Scale bars = 50 μm. Original magnification, ×400. *P < 0.05, **P < 0.01.

Article Snippet: In addition, CD68, LY6, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling immunohistochemical staining was performed on 5 μm thick sections ( n = 3 per group) by HistoWiz (Brooklyn, NY).

Techniques: Immunohistochemical staining, Staining, Whisker Assay