[ABSTRAK
Latar belakang: Prematuritas merupakan salah satu kelainan yang masih menjadimasalah global. Kejadian prematuritas tidak hanya terjadi di negara berkembangtetapi juga di negara maju. Beberapa kondisi ibu hamil dapat memicu keadaanhipoksia dalam rahim sehingga menyebabkan kelahiran prematur. Keadaanplasenta menggambarkan kesejahteraan janin intra uteri. Kondisi hipoksia selulermemicu ekspresi HIF-1α yang menjadi faktor transkripsi bagi CA9 sebagaipenanda hipoksia. Penelitian ini bertujuan menganalisis pengaruh hipoksiaterhadap plasenta prematur.Metode: Sampel menggunakan plasenta prematur yang hipoksia (H) dan nonhipoksia(N) sebagai kontrol. Parameter yang dinilai adalah struktur histologisplasenta (Hematoksilin-Eosin), regulator hipoksia HIF-1α (imunohistokimia), danpenanda hipoksia CA9 (ELISA).Hasil: Penilaian struktur histologis menunjukkan adanya perbedaan jumlahpembuluh darah fetus antara kedua kelompok secara bermakna, dimana padakelompok hipoksia jumlah pembuluh darah fetus lebih banyak dibandingkankelompok non-hipoksia. Distribusi intensitas ekspresi HIF-1α kedua kelompokjuga berbeda bermakna. Rerata kadar CA9 kedua kelompok tidak berbedabermakna, namun terdapat kecenderungan rerata kadar CA9 kelompok hipoksialebih tinggi 28% dibandingkan yang non-hipoksia.Kesimpulan: Pengaruh hipoksia terhadap plasenta prematur pada tingkatmolekuler berupa stabilitas protein HIF-1α yang menyebabkan peningkatanjumlah pembuluh darah fetus dan terjadi kecenderungan peningkatan sintesisprotein CA9.
ABSTRACT
Background: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein.;Background: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein., Background: Prematurity is a disorder that is still a global problem. Incidence ofprematurity is a problem in developing and also in developed countries. Certaincondition accompanying pregnancies may trigger uterine hypoxia, causingpremature birth. The placental condition is related with the intra-uterine fetalcondition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead tostabilization of HIF-1α protein, a transcription factor of CA9. This study aimed toanalyze the effect of hypoxia on the premature placenta.Methods: Samples from hypoxic premature placenta (H) and non-hypoxicpremature placenta (N) were collected. Parameters assessed were histologicalstructure of the placenta (Hematoxylin-Eosin), expression of HIF-1α(immunohistochemistry) and the level of CA9 (ELISA).Results: Assessment of histological structure showed the number of fetal bloodvessels were differed significantly between the two group, wherein the hypoxiagroup was more than the non-hypoxia. The distributions of HIF-1α expressionbetween the two groups were also differed significantly. The average level of CA9between two groups were not significant, but there is a tendency of higher level ofCA9 in the hypoxia group (28% higher compared to the non-hypoxia group).Conclusion: It is concluded that the effect of the hypoxia on premature placentain this study occured at molecular level and lead to HIF-1α protein stability thatcauses an increase of the number of fetal blood vessel and synthesis of CA9protein.] |
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