Objective       To determine the expression profile of glia cells missing 2 (Gcm2) in rats during the course of secondary hyperparathyroidism and its relationship with parathyroid cell proliferation.       Methods       A total of 42 female SD rats

at an age of 6 to 8 weeks

weighting 180 to 220 g

were randomly divided into sham-operation group (n=6) and hyperparathyroidism group (n=36). Rat model of secondary hyperparathyroidism

was established by 5/6 nephrectomy combined with following high phosphorus feeding. Parathyroid glands and serum were collected after 6 rats of the model group were killed at the following intervals of 1

4

7

14

21 and 28 d

respectively. Serum level of intact parathyroid hormone (i-PTH) was detected by ELISA. The expression of Gcm2 at mRNA and protein levels was observed by real-time PCR and Western blotting

respectively. Parathyroid cell proliferation were observed by immunohistochemical assay.       Results       Compared with the sham-operation group

i-PTH levels were significantly elevated at all time points in the model group (

P

0.01). In the model group

the mRNA expression of Gcm2 was increased gradually with time elapse

though without significant difference in the days 1

4 and 7

but significantly higher in the day 14 (

P

0.01)

and reached the highest level in the day 21

which were increased by 9.92 fold when compared with sham-operation group (P0.01)

and then the level was decreased mildly in the day 28 (

P

0.01). While

the expression of Gcm2 protein was slightly weakened in the first day

then gradually elevated in the day 4

and continued to raise till the highest level in the day 21 except a little fluctuation in the day 7

but the level was also decreased in the day 28 (

P

0.01). The proliferative rate of parathyroid cells was very high in the day 1 (

P

0.01)

and reached the peak in the day 4 (

P

0.01)

and then became declined till to the normal rate since the day 14.       Conclusion      In the pathogenesis of secondary hyperparathyroidism

Gcm2 expression and parathyroid cell proliferation showed an opposite trend. The interaction between them may partly contribute to the hyperfunction of the parathyroid.