Structural measurements and vessel density of spectraldomain optic coherence tomography in early,moderate,and severe primary angle-closure glaucoma

AIM:To compare the macular ganglion cell-inner plexiform layer(GCIPL)thickness,retinal nerve fiber layer(RNFL)thickness,optic nerve head(ONH)parameters,and retinal vessel density(VD)measured by spectral-domain optical coherence tomography(SD-OCT)and analyze the correlations between them in the early,moderate,severe primary angle-closure glaucoma(PACG)and normal eyes.METHODS:Totally 70 PACG eyes and 20 normal eyes were recruited for this retrospective analysis.PACG eyes were further separated into early,moderate,or severe PACG eyes using the Enhanced Glaucoma Staging System(GSS2).The GCIPL thickness,RNFL thickness,ONH parameters,and retinal VD were measured by SD-OCT,differences among the groups and correlations within the same group were calculated.RESULTS:The inferior and superotemporal sectors of the GCIPL thickness,rim area of ONH,average and inferior sector of the retinal VD were significantly reduced(all P<0.05)in the early PACG eyes compared to the normal and the optic disc area,cup to disc ratio(C/D),and cup volume were significantly higher(all P<0.05);but the RNFL was not significant changes in early and moderate PACG.In severe group,the GCIPL and RNFL thickness were obvious thinning with retinal VD were decreasing as well as C/D and cup volume increasing than other three groups(all P<0.01).In the early PACG subgroup,there were significant positive correlations between retinal VD and GCIPL thickness(except superonasal and inferonasal sectors,r=0.573 to 0.641,all P<0.05),superior sectors of RNFL thickness(r=0.055,P=0.049).More obvious significant positive correlations were existed in moderate PACG eyes between retinal VD and superior sectors of RNFL thickness(r=0.650,P=0.022),and temporal sectors of RNFL thickness(r=0.740,P=0.006).In the severe PACG eyes,neither GCIPL nor RNFL thickness was associated with retinal VD.CONCLUSION:The ONH damage and retinal VD loss appears earlier than RNFL thickness loss in PACG eyes.As the PACG disease progressed from the early to the moderate stage,the correlations between the retinal VD and RNFL thickness increases.

Expressions of type I collagen, α2 integrin and β1 integrin in sclera of guinea pig with defocus myopia and inhibitory effects of bFGF on the formation of myopia

AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the formation and development of myopia by upregulating the expression of type I collagen, α2 integrin and β1 integrin. METHODS:After 14 days of treatment, the refractive state and axial length were measured and the levels of type I collagen, α2 integrin and β1 integrin were assayed in the posterior sclerae of groups of guinea pigs that wore a monocular-7D polymethylmethacrylate (PMMA) lens or had -7D lens wear followed by the peribulbar injection of Phosphate Buffer Solution (PBS) or bFGF. The untreated fellow eye served as a control. Guinea pigs with no treatment served as normal group. ·RESULTS:The results showed that 14 days of monocular defocus increased axial eye length and refraction, while bFGF delivery inhibited them markedly. Further, it was also found that the monocular-7D lens could decrease the levels of type I collagen, α2 integrin and β1 integrin expressions, while, unlike PBS, bFGF increased them significantly in comparison to contralateral control eyes and normal eyes. CONCLUSION:bFGF can prevent the formation anddevelopment of defocus myopia by upregulating the expressions of type I collagen, α2 integrin and β1 integrin. Taken together, our results demonstrate that bFGF promotes sclera remodeling to prevent myopia in guinea pigs.

Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury

Our previous study has shown that the transcription factor Krüppel-like factor 7(KLF7) promotes peripheral nerve regeneration and motor function recovery after spinal cord injury.KLF7 also participates in traumatic brain injury,but its regulatory mechanisms remain poorly understood.In the present study,an HT22 cell model of traumatic brain injury was established by stretch injury and oxygenglucose deprivation.These cells were then transfected with an adeno-associated virus carrying KLF7(AAV-KLF7).The results revealed that,after stretch injury and oxygen-glucose deprivation,KLF7 greatly reduced apoptosis,activated caspase-3 and lactate dehydrogenase,downregulated the expression of the apoptotic markers B-cell lymphoma 2(Bcl-2)-associated X protein(Bax) and cleaved caspase-3,and increased the expression of βIII-tubulin and the antiapoptotic marker Bcl-2.Furthermore,KLF7 overexpression upregulated Janus kinase 2(JAK2) and signal transducer and activator of transcription 3(STAT3) phosphorylation in HT22 cells treated by stretch injury and oxygenglucose deprivation.Immunoprecipitation assays revealed that KLF7 directly participated in the phosphorylation of STAT3.In addition,treatment with AG490,a selective inhibitor of JAK2/STAT3,weakened the protective effects of KLF7.A mouse controlled cortical impact model of traumatic brain injury was then established.At 30 minutes before modeling,AAV-KLF7 was injected into the ipsilateral lateral ventricle.The protein and m RNA levels of KLF7 in the hippocampus were increased at 1 day after injury and recovered to normal levels at 3 days after injury.KLF7 reduced ipsilateral hippocampal atrophy,decreased the injured cortex volume,downregulated Bax and cleaved caspase-3 expression,and increased the number of 5-bromo-2'-deoxyuridine-positive neurons and Bcl-2 protein expression.Moreover,KLF7 transfection greatly enhanced the phosphorylation of JAK2 and STAT3 in the ipsilateral hippocampus.These results suggest that KLF7 may protect hippocampal neurons after traumatic brain injury through activation of the JAK2/STAT3 signaling pathway.The study was approved by the Institutional Review Board of Mudanjiang Medical University,China(approval No.mdjyxy-2018-0012) on March 6,2018.