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Protection of retina by mini-αA in NaIO3-induced retinal pigment epithelium degeneration mice.

Zhang J, Zhao X, Cai Y, Li Y, Yu X, Lu L - Int J Mol Sci (2015)

Bottom Line: Further investigation into how mini-αA provided protection against NaIO3-induced RPE cell apoptosis showed that mini-αA reduced NaIO3-induced RPE cell apoptosis and autophagy.In addition, unfolded protein response was also involved in the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis. mini-αA can antagonize RPE cell apoptosis induced by NaIO3.A possible mechanism is by inhibition of apoptosis by repressing autophagy and endoplasmic reticulum stress.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China. zhjinglin@126.com.

ABSTRACT

Background: Studies have shown that mini-αA can protect retinal pigment epithelium (RPE) cells from apoptosis. However, no in vivo study concerning the anti-apoptotic function of mini-αA has been conducted yet.

Methods: MTT assay, HE staining and TUNEL assay were used to assess levels of cells, and an animal model was established to examine the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis. Western blot analysis and RT-qPCR were performed to explore the possible mechanism of mini-αA's protective function against NaIO3-induced RPE cell apoptosis.

Results: RESULTS from in vivo and animal experiments showed that mini-αA antagonized NaIO3-induced RPE cell apoptosis. Further investigation into how mini-αA provided protection against NaIO3-induced RPE cell apoptosis showed that mini-αA reduced NaIO3-induced RPE cell apoptosis and autophagy. In addition, unfolded protein response was also involved in the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis.

Conclusions: mini-αA can antagonize RPE cell apoptosis induced by NaIO3. A possible mechanism is by inhibition of apoptosis by repressing autophagy and endoplasmic reticulum stress.

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Related in: MedlinePlus

mini-αA treatment protect the injuries induced by NaIO3. (A) HE staining of retina two weeks after mouse model of NaIO3-induced retinal degeneration was established. (Control) Retina of normal control group, whose layers were organized and cellular stratification neat; (NaIO3) Retina of NaIO3 group; (mini-αA group) Retina of mini-αA group. GCL: ganglion cell layer, IPL: internal plexiform layer, INL: internal nuclear layer, EPL: external plexiform layer, ENL: external nuclear layer, PRL: photoreceptor layer, RPE: retinal pigmented epithelium. Arrows indicated the retina damages caused by NaIO3. Thickness reduction was seen in GCL, EPL, PRL. RPE layers were discontinuous. Magnification: 400×; (B) Nuclei number of INL and ENL was counted. Significant reduction of nuclei number of INL and ENL was observed in NaIO3 group compared to the control and the mini-αA group mini-αA treatment reversed the nuclei number reduction. Quantification of nuclei number was performed with six independent experiments. * p < 0.05 vs. INL of the control; # p < 0.05 vs. ENL of the control; ^ p < 0.05 vs. INL of the NaIO3 group; Δ p < 0.05 vs. ENL of the NaIO3 group.
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ijms-16-01644-f002: mini-αA treatment protect the injuries induced by NaIO3. (A) HE staining of retina two weeks after mouse model of NaIO3-induced retinal degeneration was established. (Control) Retina of normal control group, whose layers were organized and cellular stratification neat; (NaIO3) Retina of NaIO3 group; (mini-αA group) Retina of mini-αA group. GCL: ganglion cell layer, IPL: internal plexiform layer, INL: internal nuclear layer, EPL: external plexiform layer, ENL: external nuclear layer, PRL: photoreceptor layer, RPE: retinal pigmented epithelium. Arrows indicated the retina damages caused by NaIO3. Thickness reduction was seen in GCL, EPL, PRL. RPE layers were discontinuous. Magnification: 400×; (B) Nuclei number of INL and ENL was counted. Significant reduction of nuclei number of INL and ENL was observed in NaIO3 group compared to the control and the mini-αA group mini-αA treatment reversed the nuclei number reduction. Quantification of nuclei number was performed with six independent experiments. * p < 0.05 vs. INL of the control; # p < 0.05 vs. ENL of the control; ^ p < 0.05 vs. INL of the NaIO3 group; Δ p < 0.05 vs. ENL of the NaIO3 group.

Mentions: To further validate that mini-αA provides protection against NaIO3-induced retinal degeneration, this study established a mouse model of NaIO3-induced retinal degeneration. HE staining was performed on retinal Sections two weeks after the model was successfully established. Results showed that, compared with those of the normal mice, the retinas of the mice with NaIO3-induced retinal degeneration were obviously thinner, with thinning of the photoreceptor layer being most evident, and the layers of the retina were disorganized with displaced cells. The structure of the RPE layer was not clear, and almost no RPE cells were noted. The retinas of mini-αA group were slightly thinner than those of normal mice, but thicker than retinas induced by NaIO3, and the cellular stratification of the retinas of mini-αA group was neater. Similar to retinas induced by NaIO3, a reduction in the thickness of the photoreceptor layer was most evident, the structure of RPE layer unclear, and almost no RPE cells were identified (Figure 2A). Quantification of nuclei of the internal nuclear layer (INL) and external plexiform layer (ENL) confirmed the protection of retinas damage caused by NaIO3 (Figure 2B). These results suggest that, in agreement with the in vitro experiment, mini-αA can protect retinas against injuries caused by NaIO3.


Protection of retina by mini-αA in NaIO3-induced retinal pigment epithelium degeneration mice.

Zhang J, Zhao X, Cai Y, Li Y, Yu X, Lu L - Int J Mol Sci (2015)

mini-αA treatment protect the injuries induced by NaIO3. (A) HE staining of retina two weeks after mouse model of NaIO3-induced retinal degeneration was established. (Control) Retina of normal control group, whose layers were organized and cellular stratification neat; (NaIO3) Retina of NaIO3 group; (mini-αA group) Retina of mini-αA group. GCL: ganglion cell layer, IPL: internal plexiform layer, INL: internal nuclear layer, EPL: external plexiform layer, ENL: external nuclear layer, PRL: photoreceptor layer, RPE: retinal pigmented epithelium. Arrows indicated the retina damages caused by NaIO3. Thickness reduction was seen in GCL, EPL, PRL. RPE layers were discontinuous. Magnification: 400×; (B) Nuclei number of INL and ENL was counted. Significant reduction of nuclei number of INL and ENL was observed in NaIO3 group compared to the control and the mini-αA group mini-αA treatment reversed the nuclei number reduction. Quantification of nuclei number was performed with six independent experiments. * p < 0.05 vs. INL of the control; # p < 0.05 vs. ENL of the control; ^ p < 0.05 vs. INL of the NaIO3 group; Δ p < 0.05 vs. ENL of the NaIO3 group.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4307325&req=5

ijms-16-01644-f002: mini-αA treatment protect the injuries induced by NaIO3. (A) HE staining of retina two weeks after mouse model of NaIO3-induced retinal degeneration was established. (Control) Retina of normal control group, whose layers were organized and cellular stratification neat; (NaIO3) Retina of NaIO3 group; (mini-αA group) Retina of mini-αA group. GCL: ganglion cell layer, IPL: internal plexiform layer, INL: internal nuclear layer, EPL: external plexiform layer, ENL: external nuclear layer, PRL: photoreceptor layer, RPE: retinal pigmented epithelium. Arrows indicated the retina damages caused by NaIO3. Thickness reduction was seen in GCL, EPL, PRL. RPE layers were discontinuous. Magnification: 400×; (B) Nuclei number of INL and ENL was counted. Significant reduction of nuclei number of INL and ENL was observed in NaIO3 group compared to the control and the mini-αA group mini-αA treatment reversed the nuclei number reduction. Quantification of nuclei number was performed with six independent experiments. * p < 0.05 vs. INL of the control; # p < 0.05 vs. ENL of the control; ^ p < 0.05 vs. INL of the NaIO3 group; Δ p < 0.05 vs. ENL of the NaIO3 group.
Mentions: To further validate that mini-αA provides protection against NaIO3-induced retinal degeneration, this study established a mouse model of NaIO3-induced retinal degeneration. HE staining was performed on retinal Sections two weeks after the model was successfully established. Results showed that, compared with those of the normal mice, the retinas of the mice with NaIO3-induced retinal degeneration were obviously thinner, with thinning of the photoreceptor layer being most evident, and the layers of the retina were disorganized with displaced cells. The structure of the RPE layer was not clear, and almost no RPE cells were noted. The retinas of mini-αA group were slightly thinner than those of normal mice, but thicker than retinas induced by NaIO3, and the cellular stratification of the retinas of mini-αA group was neater. Similar to retinas induced by NaIO3, a reduction in the thickness of the photoreceptor layer was most evident, the structure of RPE layer unclear, and almost no RPE cells were identified (Figure 2A). Quantification of nuclei of the internal nuclear layer (INL) and external plexiform layer (ENL) confirmed the protection of retinas damage caused by NaIO3 (Figure 2B). These results suggest that, in agreement with the in vitro experiment, mini-αA can protect retinas against injuries caused by NaIO3.

Bottom Line: Further investigation into how mini-αA provided protection against NaIO3-induced RPE cell apoptosis showed that mini-αA reduced NaIO3-induced RPE cell apoptosis and autophagy.In addition, unfolded protein response was also involved in the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis. mini-αA can antagonize RPE cell apoptosis induced by NaIO3.A possible mechanism is by inhibition of apoptosis by repressing autophagy and endoplasmic reticulum stress.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China. zhjinglin@126.com.

ABSTRACT

Background: Studies have shown that mini-αA can protect retinal pigment epithelium (RPE) cells from apoptosis. However, no in vivo study concerning the anti-apoptotic function of mini-αA has been conducted yet.

Methods: MTT assay, HE staining and TUNEL assay were used to assess levels of cells, and an animal model was established to examine the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis. Western blot analysis and RT-qPCR were performed to explore the possible mechanism of mini-αA's protective function against NaIO3-induced RPE cell apoptosis.

Results: RESULTS from in vivo and animal experiments showed that mini-αA antagonized NaIO3-induced RPE cell apoptosis. Further investigation into how mini-αA provided protection against NaIO3-induced RPE cell apoptosis showed that mini-αA reduced NaIO3-induced RPE cell apoptosis and autophagy. In addition, unfolded protein response was also involved in the protective effects of mini-αA against NaIO3-induced RPE cell apoptosis.

Conclusions: mini-αA can antagonize RPE cell apoptosis induced by NaIO3. A possible mechanism is by inhibition of apoptosis by repressing autophagy and endoplasmic reticulum stress.

Show MeSH
Related in: MedlinePlus