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ABSTRAKLatar belakang: Prematuritas merupakan salah satu kelainan yang masih menjadi
masalah global. Kejadian prematuritas tidak hanya terjadi di negara berkembang
tetapi juga di negara maju. Beberapa kondisi ibu hamil dapat memicu keadaan
hipoksia dalam rahim sehingga menyebabkan kelahiran prematur. Keadaan
plasenta menggambarkan kesejahteraan janin intra uteri. Kondisi hipoksia seluler
memicu ekspresi HIF-1α yang menjadi faktor transkripsi bagi CA9 sebagai
penanda hipoksia. Penelitian ini bertujuan menganalisis pengaruh hipoksia
terhadap plasenta prematur.
Metode: Sampel menggunakan plasenta prematur yang hipoksia (H) dan nonhipoksia
(N) sebagai kontrol. Parameter yang dinilai adalah struktur histologis
plasenta (Hematoksilin-Eosin), regulator hipoksia HIF-1α (imunohistokimia), dan
penanda hipoksia CA9 (ELISA).
Hasil: Penilaian struktur histologis menunjukkan adanya perbedaan jumlah
pembuluh darah fetus antara kedua kelompok secara bermakna, dimana pada
kelompok hipoksia jumlah pembuluh darah fetus lebih banyak dibandingkan
kelompok non-hipoksia. Distribusi intensitas ekspresi HIF-1α kedua kelompok
juga berbeda bermakna. Rerata kadar CA9 kedua kelompok tidak berbeda
bermakna, namun terdapat kecenderungan rerata kadar CA9 kelompok hipoksia
lebih tinggi 28% dibandingkan yang non-hipoksia.
Kesimpulan: Pengaruh hipoksia terhadap plasenta prematur pada tingkat
molekuler berupa stabilitas protein HIF-1α yang menyebabkan peningkatan
jumlah pembuluh darah fetus dan terjadi kecenderungan peningkatan sintesis
protein CA9.
ABSTRACTBackground: Prematurity is a disorder that is still a global problem. Incidence of
prematurity is a problem in developing and also in developed countries. Certain
condition accompanying pregnancies may trigger uterine hypoxia, causing
premature birth. The placental condition is related with the intra-uterine fetal
condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to
stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to
analyze the effect of hypoxia on the premature placenta.
Methods: Samples from hypoxic premature placenta (H) and non-hypoxic
premature placenta (N) were collected. Parameters assessed were histological
structure 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 blood
vessels were differed significantly between the two group, wherein the hypoxia
group was more than the non-hypoxia. The distributions of HIF-1α expression
between the two groups were also differed significantly. The average level of CA9
between two groups were not significant, but there is a tendency of higher level of
CA9 in the hypoxia group (28% higher compared to the non-hypoxia group).
Conclusion: It is concluded that the effect of the hypoxia on premature placenta
in this study occured at molecular level and lead to HIF-1α protein stability that
causes an increase of the number of fetal blood vessel and synthesis of CA9
protein.;Background: Prematurity is a disorder that is still a global problem. Incidence of
prematurity is a problem in developing and also in developed countries. Certain
condition accompanying pregnancies may trigger uterine hypoxia, causing
premature birth. The placental condition is related with the intra-uterine fetal
condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to
stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to
analyze the effect of hypoxia on the premature placenta.
Methods: Samples from hypoxic premature placenta (H) and non-hypoxic
premature placenta (N) were collected. Parameters assessed were histological
structure 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 blood
vessels were differed significantly between the two group, wherein the hypoxia
group was more than the non-hypoxia. The distributions of HIF-1α expression
between the two groups were also differed significantly. The average level of CA9
between two groups were not significant, but there is a tendency of higher level of
CA9 in the hypoxia group (28% higher compared to the non-hypoxia group).
Conclusion: It is concluded that the effect of the hypoxia on premature placenta
in this study occured at molecular level and lead to HIF-1α protein stability that
causes an increase of the number of fetal blood vessel and synthesis of CA9
protein., Background: Prematurity is a disorder that is still a global problem. Incidence of
prematurity is a problem in developing and also in developed countries. Certain
condition accompanying pregnancies may trigger uterine hypoxia, causing
premature birth. The placental condition is related with the intra-uterine fetal
condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to
stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to
analyze the effect of hypoxia on the premature placenta.
Methods: Samples from hypoxic premature placenta (H) and non-hypoxic
premature placenta (N) were collected. Parameters assessed were histological
structure 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 blood
vessels were differed significantly between the two group, wherein the hypoxia
group was more than the non-hypoxia. The distributions of HIF-1α expression
between the two groups were also differed significantly. The average level of CA9
between two groups were not significant, but there is a tendency of higher level of
CA9 in the hypoxia group (28% higher compared to the non-hypoxia group).
Conclusion: It is concluded that the effect of the hypoxia on premature placenta
in this study occured at molecular level and lead to HIF-1α protein stability that
causes an increase of the number of fetal blood vessel and synthesis of CA9
protein.]
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